Stem Cell Research & Therapy•2025•DOI: 10.1186/s13287-025-04773-w
Reproductive system disorders significantly contribute to infertility, and traditional or conventional treatments often have limited efficacy in addressing this issue. In recent years, stem cell therapy has emerged as an alternative therapeutic strategy owing to its various advantages. Human umbilical cord mesenchymal stem cells (hUC-MSCs) are pivotal in tissue repair owing to their robust proliferative capacity, potent immunomodulatory effects, low immunogenicity, and paracrine actions. Extracellular vesicles (EVs), the primary mediators of paracrine functions, exhibit therapeutic effects similar to those of hUC-MSCs. Consequently, numerous researchers have investigated the application of hUC-MSCs and their EVs in treating reproductive disorders. These cells have the potential to restore fertility by mitigating oxidative stress, excessive autophagy, and ferroptosis in tissues, while promoting the expression of anti-inflammatory factors and vascular remodeling. However, hUC-MSCs present significant limitations compared to EVs, including higher tumorigenicity and low infusion efficiency. Consequently, EVs may emerge as the primary alternative therapy, while hUC-MSCs hold promise as a therapeutic option with potential applications in regenerative medicine.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025233
This is a corrigendum to the article 'Caveolin-1-deficient fibroblasts promote migration, invasion, and stemness by activating the TGF-β/Smad signaling pathway in breast cancer cells' published in Acta Biochim Biophys Sin 54: 1587–1598. The authors identified inaccuracies in the preparation of several figures (Figure 2D, 4A, and 5A) and have replaced them with corrected versions. The errors are strictly confined to figure presentation and do not impact the underlying data, statistical analysis, or main conclusions. The authors apologize for the oversight.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2024182
Glycan-mediated recognition plays a critical role in facilitating cell-cell and cell-matrix interactions. Galectin-8 (Gal-8), classified as a ‘tandem-repeat’ type of galectin, binds to cell surface glycans to modulate various cellular functions, including cell adhesion, migration, apoptosis, pathogen recognition, autophagy, and immunomodulation. Despite the known function of Gal-8 in binding to various glycosylated proteins, only a few interactions have been reported to date. In this study, mass spectrometry is used to identify CD98hc as a novel binding partner for Gal-8. Both the N-terminal and C-terminal carbohydrate recognition domains (CRDs) of Gal-8 (Gal-8N and Gal-8C) bind to CD98hc, an interaction that is specifically inhibited by lactose but not sucrose, as confirmed by pull-down assays. The binding affinity between CD98hc and Gal-8 measured by microscale thermophoresis (MST) is 1.51 ± 0.17 μM. In addition, Gal-8N and Gal-8C have the binding affinities of 0.22 ± 0.03 μM and 10.68 ± 1.69 μM, respectively. Gal-8N and Gal-8C are both involved in the recognition and binding process of CD98hc. Furthermore, both full-length Gal-8 and its individual CRDs bind specifically to N-glycosylated glycans on CD98hc, as demonstrated by the use of tunicamycin to inhibit N-glycosylation in cells. In addition, Gal-8 and its individual CRDs can pull down glycosylated CD98hc-ED but not free CD98hc-ED in vitro, indicating that the binding of Gal-8 to glycosylated CD98hc-ED is N-glycosylation-dependent. Overall, our findings establish CD98hc as a novel binding partner for Gal-8 and provide insights for further exploration of the diverse biological functions of Gal-8.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025108
Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy with poor prognosis and limited therapeutic options. N6-methyladenosine (m6A) RNA modification plays a role in tumorigenesis, but its contributions to ESCC and the regulation of cell adhesion molecules such as Nectin-4 are not fully elucidated. In this study, we investigate the role and the regulatory mechanisms of Nectin-4 in ESCC, particularly regarding the influence of m6A modification and its downstream metabolic effects. Our study demonstrates that methyltransferase-like protein 3 (METTL3) enhances Nectin-4 mRNA stability and expression through m6A methylation in ESCC, as validated by actinomycin D assay, MeRIP-qPCR, and dual-luciferase reporter assay. Both METTL3 and Nectin-4 are highly expressed in ESCC tissues and promote malignant phenotypes such as proliferation, migration, and invasion. Further analysis identifies pantothenate esterase 1 (VNN1) as a downstream target of Nectin-4, mediating the oncogenic effects of the METTL3/Nectin-4 axis and promoting the biosynthesis of pantothenic acid and coenzyme A, thus driving ESCC progression. By integrating transcriptomic data, this study elucidates a key pathogenic mechanism in which the METTL3/Nectin-4/VNN1 axis regulates metabolic reprogramming to promote ESCC development. These findings provide new insights into the molecular pathology of ESCC and offer potential biomarkers and therapeutic targets for early screening, prognosis, and precision treatment for ESSC.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024091
Hepatitis E virus (HEV) is the major pathogen of viral hepatitis. Immunocompromised individuals infected by HEV are prone to chronic hepatitis and increase the risk of hepato-cellular carcinoma (HCC). Inhibitor of growth family member 5 (ING5) is a tumor suppressor that is expressed at low levels in cancer tumors or cells. However, the underlying relationship between ING5 and HEV infection is unclear. In the present study, acute and chronic HEV animal models are used to explore the interaction between ING5 and HEV. Notably, the expression of ING5 is significantly increased in both the livers of acute HEV-infected BALB/c mice and chronic HEV-infected rhesus macaques. In addition, the relationship between HEV infection and ING5 expression is further identified in human hepatoma (HepG-2) cells. In conclusion, HEV infection strongly upregulates ING5 expression both in vivo and in vitro, which has significant implications for further understanding the pathogenic mechanism of HEV infection.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025038
Hepatocellular carcinoma (HCC) is a highly fatal form of malignancy that seriously threatens patient survival. The global 5-year survival rate for HCC patients ranges from 15% to 19%, and nearly 80% of patients are diagnosed at an advanced stage. Therefore, exploring the mechanism of HCC development and identifying biomarkers and therapeutic targets for HCC are vital. MicroRNAs (miRNAs), a class of noncoding single-stranded RNAs, are 20–24 nucleotides (nt) long. They play pivotal roles in modulating the progression of diverse diseases. The specific role of miR-32-5p in the development of HCC remains unclear. In this study, qRT-PCR is utilized to precisely determine the downregulated expression levels of miR-32-5p in HCC. Subsequently, functional analysis reveals the suppressive role of miR-32-5p in modulating the proliferative and migratory capabilities of HCC cells. Glycogen synthase kinase 3β (GSK3β) has emerged as a potential target of miR-32-5p, which is confirmed through a dual-luciferase reporter assay. Notably, the expression of GSK3β in HCC tissue specimens is negatively correlated with the abundance of miR-32-5p, and patients with high GSK3β expression have shorter survival time. Furthermore, the targeted downregulation of GSK3β remarkably impedes the proliferation and migration of tumor cells. This study suggests that miR-32-5p inhibits the proliferation and migration of HCC through regulating the GSK3β/NF-κB signaling pathway. Therefore, this study reveals that miR-32-5p exerts its suppressive effect on HCC progression, suggesting that it is a promising target for both diagnostic and targeted therapeutic interventions against HCC.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2024162
Hepatic fibrosis (HF) is an abnormal reparative response of the liver to chronic injury and is histologically reversible. In recent years, increasing interest has been given to changes in m6A in liver disease. In this study, we explore the role of the m6A-modified reading protein YTHDF2 in HF and its regulatory mechanism. The HF mouse model is generated through CCl4 injection, and the cell model is via TGF-β stimulation. The liver tissues are subjected to hematoxylin-eosin, Masson, and α-SMA immunohistochemical staining. Reactive oxygen species (ROS) and iron levels are examined via relevant kits. Quantitative real-time PCR, immunofluorescence staining, and western blot analysis were conducted to measure the YTHDF2 and ACSL4 levels. RNA immunoprecipitation, methylated RNA immunoprecipitation, RNA pull-down, and polysome fractionation were performed to understand the regulatory mechanism by which YTHDF2 affects ACSL4. The results show that YTHDF2 is highly expressed after HF induction, and the inhibition of YTHDF2 reduces fibrosis as well as ROS and iron levels. In vitro, overexpression of YTHDF2 increases hepatic stellate cell activation, as well as ROS and iron levels, and this effect is blocked by the silencing of ACSL4. YTHDF2 acts as a regulator of ACSL4 expression and is involved in m6A modification. In addition, in vivo experiments indicate that overexpression of ACSL4 reverses the attenuating effect of YTHDF2 interference on HFs. Therefore, YTHDF2 mediates the expression of the ferroptosis marker protein ACSL4 in an m6A-dependent manner, thereby affecting HF.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025124
Preeclampsia (PE) involves complex metabolic-inflammatory interactions, yet the mechanistic links among glycolysis, protein lactylation, and pyroptosis in placental pathogenesis remain undefined. In this study, we explore their tripartite relationship with PE development by combining bioinformatics analysis of PE-associated transcriptomes with experimental validation using placental tissues from PE patients and healthy controls. To elucidate the underlying mechanism, we utilize in vitro models involving hypoxic endothelial cell cultures, pharmacological glycolysis inhibition via 2-deoxyglucose, and genetic modulation of hexokinase 2 (HK2) expressions through siRNA silencing and plasmid-based overexpression. Molecular profiling is used to assess the expressions of key glycolytic enzymes, lactylation markers, and pyroptosis-related factors. Compared with control placental tissues, PE placental tissues present significantly higher expressions of glycolytic enzymes, elevated protein lactylation levels, and increased pyroptosis markers. Similarly, hypoxic endothelial cells exhibit coordinated upregulation of these three pathways. Notably, pharmacological glycolysis inhibition significantly reduces both lactylation and pyroptosis levels. Genetic experiments further demonstrate that HK2 silencing decreases glycolytic activity, subsequently attenuating lactylation and pyroptosis, whereas HK2 overexpression has opposite effects, underscoring its central regulatory role in this metabolic-inflammatory axis. Collectively, these findings indicate that HK2-mediated glycolysis drives placental vascular endothelial lactylation and pyroptosis, revealing a novel mechanistic pathway in PE pathophysiology.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2023286
Thioredoxin-interacting protein (TXNIP) is a crucial thioredoxin-binding protein that is recognized as a tumor suppressor in diverse malignancies, such as breast cancer, lung cancer, hepatocellular carcinoma, and thyroid cancer. However, the specific role and molecular mechanisms of TXNIP in the pathogenesis and progression of pancreatic cancer cells have not been determined. In this study, we investigate the relationship between TXNIP expression and overall survival prognosis in pancreatic cancer patients. Mechanistic studies are conducted to reveal the role of TXNIP in pancreatic cancer cell proliferation, migration, and regulation during malignancy. Our findings indicate that patients with high TXNIP expression have a more favorable prognosis. In vitro experiments with pancreatic cell lines show that overexpression of TXNIP suppresses the proliferation and migration of pancreatic cancer cells. Furthermore, we find that TXNIP inhibits the activation of the MAPK signaling pathway, thereby decreasing the malignant potential of pancreatic cancer. In conclusion, our study reveals TXNIP as a promising new predictive marker and therapeutic target for pancreatic cancer.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2024173
Pyroptosis, a newly discovered form of programmed cell death, is involved in the occurrence, development and drug resistance of a variety of tumors and has attracted increasing attention in recent years. LINC00365 is a novel lncRNA that has rarely been reported before. We previously reported that LINC00365 expression in colorectal cancer is closely associated with poor patient outcomes. Additionally, LINC00365 was confirmed to be positively correlated with miR-221-5p, and miR-221-5p is negatively correlated with gasdermin-D (GSDMD) in colorectal cancer tissues. Bioinformatics analysis and luciferase reporter gene experiments revealed that GSDMD is the target gene of miR-221-5p. Cell function experiments and nude mouse tumor transplantation assays confirmed that LINC00365 could regulate the expressions of pyroptosis-related proteins such as Caspase-1, Caspase-11, NLRP3 and GSDMD. RNA pulldown and RNA immunoprecipitation experiments further elucidated the mechanism by which LINC00365 regulates miR-221-5p. In the present study, we observe that LINC00365 promotes the expression of miR-221-5p by binding to the Dicer enzyme to inhibit GSDMD and plays an antipyroptotic role. Our findings suggest that LINC00365 may serve as a molecular biomarker for estimating the prognosis of patients with colorectal cancer and as a potential therapeutic target for colorectal cancer.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024051
The epicardium is integral to cardiac development and facilitates endogenous heart regeneration and repair. While miR-194-3p is associated with cellular migration and invasion, its impact on epicardial cells remains uncharted. In this work we use gain-of-function and loss-of-function methodologies to investigate the function of miR-194-3p in cardiac development. We culture embryonic epicardial cells in vitro and subject them to transforming growth factor β (TGF-β) treatment to induce epithelial-mesenchymal transition (EMT) and monitor miR-194-3p expression. In addition, the effects of miR-194-3p mimics and inhibitors on epicardial cell development and changes in EMT are investigated. To validate the binding targets of miR-194-3p and its ability to recover the target gene-phenotype, we produce a mutant vector p120-catenin-3′UTR-MUT. In epicardial cells, TGF-β-induced EMT results in a notable overexpression of miR-194-3p. The administration of miR-194-3p mimics promotes EMT, which is correlated with elevated levels of mesenchymal markers. Conversely, miR-194-3p inhibitor attenuates EMT. Further investigations reveal a negative correlation between miR-194-3p and p120-catenin, which influences β-catenin level in the cell adhesion pathway. The suppression of EMT caused by the miR-194-3p inhibitor is balanced by silencing of p120-catenin. In conclusion, miR-194-3p directly targets p120-catenin and modulates its expression, which in turn alters β-catenin expression, critically influencing the EMT process in the embryonic epicardial cells via the cell adhesion mechanism.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024146
Eukaryotic gene expression is regulated at multiple levels, aiding in maintaining normal phenotypes and environmental adaptability. Transcriptional regulation complexity has been extensively studied using high-throughput sequencing, and previous studies have shown that different transcript isoforms can be produced through complex regulatory mechanisms via large-scale RNA sequencing. Additionally, translational regulation, which significantly influences gene expression, is controlled by complex mechanisms [1]. The untranslated regions (UTRs) of eukaryotic mRNA, encompassing the 5′ UTR, 3′ UTR and polyadenylation tail (polyA), are pivotal for translational regulation, with distinct cis-regulatory elements in the 5′ UTR and 3′ UTR of various transcript isoforms, leading to substantial variations in translational regulation across transcripts. To shed light on translational regulation, previous studies have performed isolation of ribosome-associated poly-adenylated RNAs (i.e., translatome) and deep sequencing for mRNA translation [2]. Polysome profiling is the most common method used to study translatome, which can enable the isolation of full-length translated mRNAs, thereby facilitating the identification of UTRs, assessment of selective translation, and comprehension of the regulatory mechanisms underlying gene expression [2]. Drosophila embryonic development progresses very rapidly and requires precise regulation of the transcription and translation of a large number of genes to ensure normal gene expression. Although Drosophila has been extensively studied as a model organism, the specific interplay between transcription and translation during embryonic development stages is not yet fully understood. To investigate the dynamic regulation of gene expression during Drosophila embryogenesis, we conducted transcriptome and translatome co-profiling on early (0‒4 h) embryos and S2R+ cells, a cell line derived from late embryonic stages of Drosophila melanogaster [3], to compare the differences in translational regulation at the gene and transcript isoform levels. S2R+ cell culture and early (0–4 h) embryo collection were performed (see Supplementary Methods) to compare transcriptome and translatome profiling, as shown in Supplementary Figure S1. Cytosolic RNA and ribosome-associated RNA were isolated from embryos [4] and S2R+ cells, which were used for constructing RNA-Seq libraries. Four libraries were generated for RNA-seq (see Supplementary Methods), consisting of two cytosolic RNA libraries and two ribosome-associated RNA libraries (Supplementary Figure S1A,B). The strand-specific RNA-seq libraries were prepared using the Illumina TruSeq Stranded mRNA Sample Preparation Kit (Illumina, San Diego, USA). The library was sequenced on the Illumina HiSeq X Ten System. We employed Trimmomatic [5] to remove low-quality reads, which resulted in approximately 89 million, 76 million, 72 million, and 56 million clean reads for the transcriptome and translatome of the early embryos and S2R+ cells, respectively. These reads were then mapped to the Drosophila genome (UCSC dm6) using HISAT2 [6]. The unique mapped reads ratio ranges from 94% to 85% and reads mapped to rRNA were less than 6% (Supplementary Table S1), indicating the high quality of the four RNA-seq libraries. Using StringTie [7], 33,470 transcripts were assembled for four mapping sequencing libraries, which revealed an average of 1.9 transcribed transcripts and 1.8 translated transcripts per gene (Supplementary Table S1), suggesting the usage of transcript isoforms widely existed in both transcription and translation of Drosophila embryos. To explore the divergence of the transcriptome during Drosophila development, we compared the transcriptome of the early embryos and S2R+ cells to identify genes with |log2(fold change)| ≥1, FPKM ≥1 in at least one condition, and adjusted P value ≤0.001. In total, we identified 2267 differentially expressed genes (DEGs) from 8815 genes. Among these DEGs, 2147 genes showed higher expression levels in the embryos, while 120 genes showed higher expression levels in S2R+ cells (Figure 1A and Supplementary Figure S2A). To investigate the underlying functional mechanism, we performed enrichment analysis to identify DEG-enriched pathways (Supplementary Table S2). Interestingly, the top 10 enriched pathways are related to morphogenesis an
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21242
BACKGROUND: Bone metabolism disorders can cause the occurrence of bone-related diseases, and forkhead box transcription factor O3 (FoxO3a) can affect the processes of proliferation, differentiation and apoptosis of bone tissue cells by regulating oxidative stress and autophagy levels, and thereby regulate the bone metabolism. OBJECTIVE: To systematically analyze the relevant research literature on the regulation of bone metabolism by FoxO3a and its mechanism of action in bone diseases and to provide a reference for subsequent studies targeting FoxO3a in the treatment of bone diseases. METHODS: Literature searches were conducted using the following strategies: CNKI (China National Knowledge Infrastructure): SU=FoxO3a OR SU=Foxo3 OR SU=Forkhead box O3 OR SU=AND SU=Forkhead box transcription factor O3) AND SU=bone; WanFang Medical Database: Subject:("FoxO3a") OR Subject:("Foxo3") OR Subject:("Forkhead box O3") OR Subject:("Forkhead box transcription factor O3") AND Subject:("bone"); PubMed: ((FoxO3a) OR (Foxo3) OR (Forkhead box O3))AND ((bone) OR (Skeleton)). Outdated, repetitive, low-quality, and irrelevant studies were excluded, and 56 articles were finally included for review. RESULTS AND CONCLUSION: ①FoxO3a and bone marrow mesenchymal stem cells: FoxO3a can promote the formation of osteogenic lineage and promote early osteogenic differentiation by activating autophagy. Meanwhile, FoxO3a exhibits antioxidant properties in bone marrow mesenchymal stem cells, protecting cells from oxidative stress-induced senescence. ②FoxO3a and osteoblasts: FoxO3a can inhibit osteogenesis by interfering with the Wnt/β-catenin pathway in osteoblasts, while it can activate antioxidant enzymes to protect mature osteoblasts. FoxO3a can promote the proliferation of osteoprogenitor cells and promote osteogenic differentiation by activating autophagy. ③FoxO3a and osteoclasts: FoxO3a expression can resist oxidative stress and activate autophagy to inhibit osteoclastogenesis. ④FoxO3a and osteocytes: FoxO3a can protect osteocytes through antioxidant effects, and can also reduce bone loss by inhibiting p16 and p53 signaling pathways and inhibiting senescence-associated secretory phenotype. ⑤FoxO3a and chondrocytes: FoxO3a plays a protective role in chondrocytes in osteoarthritis, inhibiting chondrocyte breakdown or apoptosis, promoting chondrocyte extracellular matrix synthesis, and inhibiting chondrocyte hypertrophy; however, high co-expression of FoxO3a and Runt-related transcription factor 1 in chondrocytes promotes early chondrogenesis and terminal hypertrophy of chondroprogenitor cells. ⑥FoxO3a affects bone metabolism by participating in processes such as oxidative stress resistance and regulation of autophagy, and participates in the pathological processes of various bone-related diseases.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21417
BACKGROUND: The anterior transpedicular screw fixation system can achieve adequate decompression and strong fixation in a single anterior surgery. However, due to its unique anatomical structure, the risk of screw placement is relatively high. Previous domestic and international scholars have confirmed the feasibility of this approach through anatomical measurements, but there are some drawbacks such as relatively small sample sizes, difficulties in locating the pedicle axis, and limitations in measurement methods. OBJECTIVE: To perform morphological measurements of the adult cervical spine based on imaging to provide anatomical guidance for anterior transpedicular pedicle screw fixation. METHODS: 3D CT scan data of 50 adult cervical vertebrae were imported into the Mimics system for 3D reconstruction. Morphological data were measured, including pedicle axis distance, pedicle width, pedicle height, pedicle horizontal axial angle, pedicle sagittal angle, distance from the entry point in the transverse plane, distance to the entry point in the sagittal plane, axial vertebral length and axial pedicle length. RESULTS AND CONCLUSION: (1) Positioning of nail entry points: C3 and C4 were located on the opposite side of the median sagittal plane of the vertebral body, with distances from the median sagittal line of approximately 2.060 mm and 2.310 mm. C5 could be located on the same side of the median sagittal line as or opposite to the median sagittal line, with an average value of approximately 1.224 mm. C6-C7 were located on the same side of the body, with distances of 1.132 mm and 2.538 mm from the midline; the distance from the upper endplate increased gradually from C3 to C7, with average values ranging from 2.362 to 7.350 mm. (2) Direction of nail entry: the transverse angle increased gradually from C3 to C4 (46.32°-47.36°) and decreased from C5 to C7 (44.03° to 37.80°); the sagittal angle required caudal deviation for C3-C4 (95.75° and 100.93°) and cephalad deviation for C5-C7 (104.38°, 110.34°, and 104.86°). (3) There were no significant differences in entry point location and direction between genders or sides (P > 0.05). For screw selection, except for individual patients with cervical developmental abnormalities, for most subaxial cervical pedicle screws, it is safe and reliable to choose screws at least 30 mm long and 4.0 mm in diameter for males, and at least 28 mm long and 3.5 mm in diameter for females. (4) Morphological measurements confirmed that anterior transpedicular screw fixation of the subaxial cervical spine is feasible, but individualized principles should be followed to formulate personalized fixation plans.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21367
BACKGROUND: Extracorporeal shock wave therapy, as a non-invasive and non-invasive treatment technique, is widely used in various fields. Currently, there is no systematic analysis of the latest research status, hot topics, and development trends in this field. OBJECTIVE: To analyze the research status, hotspots, and trends of extracorporeal shock wave therapy using bibliometric visualization software over the past 10 years. METHODS: Relevant literature in the field of extracorporeal shock wave therapy was retrieved from the Web of Science core database from January 1, 2015 to December 31, 2024. CiteSpace was used for analyzing publication volume, collaborations among countries/regions, institutions, and authors, citation analysis of journals and co-cited literature. Additionally, keyword co-occurrence, clustering, and burst analyses were conducted, and visualized knowledge maps were generated. RESULTS AND CONCLUSION: A total of 1 641 articles were included. The number of publications in the field of extracorporeal shock wave therapy is generally on the rise over the past 10 years. China, the United States, and Italy are the top three countries in terms of publication volume, while Chang Gung University, the University of California, and Harvard University are the top three research institutions. A total of 280 journals published articles related to extracorporeal shock wave therapy, among which Clinical Orthopaedics and Related Research was the most cited journal, and PLoS One had the highest centrality. The author with the highest publication volume was Wang, Ching-Jen from Chang Gung University, and there was little collaboration among high-yield authors and their research groups. The hot keywords in this field were mainly double-blind, pain, erectile dysfunction, plantar fasciitis, lateral epicondylitis, etc. Burst keywords included rabbit, ischemia, myocardial infarction, fasciopathy, muscle spasm, and erectile function, showing diversified research directions. Extracorporeal shock wave therapy is a non-invasive and safe treatment method. Pain management, musculoskeletal system diseases, and urological-related diseases are the research hotspots in the field of extracorporeal shock wave therapy in the past 10 years, and research on related mechanisms is also a focus of interest. Future research directions may focus on standard parameter research and long-term efficacy verification of extracorporeal shock wave therapy.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21351
BACKGROUND: Multiple chronic liver diseases that fail to heal will progress to the stage of liver fibrosis. If not treated in a timely manner, they will eventually develop into liver cancer, severely threatening the safety of patients' lives. However, there is currently no specific drug for the treatment of liver fibrosis. Recent studies have demonstrated that mesenchymal stem cell therapy has significant advantages over traditional treatment protocols, providing a new direction for the treatment of liver fibrosis. OBJECTIVE: To review the mechanisms of action of mesenchymal stem cells and their derivatives in the treatment of liver fibrosis. METHODS: The Chinese and English keywords "mesenchymal stem cells, mesenchymal stromal cells, MSCs, liver fibrosis, hepatic fibrosis, hepatocyte death, liver cell death, hepatocyte-like cells, immunomodulation, macrophage, hepatic stellate cells, clinical trials, clinical studies" were used and searched in CNKI and PubMed databases, a total of 81 eligible articles were selected for this review. RESULTS AND CONCLUSION: Through summarizing existing studies, the mechanisms by which mesenchymal stem cells and their derivatives exert anti-fibrotic effects and delay disease progression have been identified. These specific mechanisms include reducing hepatocyte death, differentiating into hepatocyte-like cells, regulating immune responses, and inhibiting hepatic stellate cell activation, confirming that mesenchymal stem cells and their derivatives can serve as a new direction for the treatment of liver fibrosis-related diseases.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21497
BACKGROUND: Recent studies have demonstrated that mechanotransduction plays a critical role in the pathological processes of neurological disorders. PIEZO channels, as key mechanosensitive ion channels, serve as core mediators in sensing and transducing mechanical signals. However, a systematic review of their specific roles across various neurological diseases is relatively lacking. OBJECTIVE: To explore the roles and molecular mechanisms of PIEZO1 and PIEZO2 channels in central and peripheral nervous system diseases, and to evaluate their potential as therapeutic targets. METHODS: A literature search was conducted in PubMed, Web of Science, CNKI, WanFang, and VIP databases from January 2010 to May 2025. English search terms included 'central nervous system diseases', 'Central Nervous System Disorder', 'CNS Disease', 'CNS Diseases', 'Central Nervous System Disorders', 'neurodegenerative disease', 'Autonomic Nervous System Diseases', 'Brain Diseases', 'Central Nervous System Infections', 'High Pressure Neurological Syndrome', 'Spinal Cord Diseases', 'PIEZO1 Channel', 'PIEZO2 Channel', 'PIEZO Channel'; Chinese search terms included '神经系统疾病', '中枢神经系统疾病', 'PIEZO1', 'PIEZO2', 'PIEZO'. A combination of subject headings and free words was used. Based on inclusion and exclusion criteria, 60 English articles were finally included for systematic analysis and classified by disease type. RESULTS AND CONCLUSION: ①PIEZO1 is highly expressed in glioma and correlates with malignancy and poor prognosis; calcium influx promotes tumor proliferation and remodeling of microenvironment stiffness, driving tumor progression. ②In intracerebral hemorrhage, activation of neuronal PIEZO2 promotes iron transporter expression, increases intracellular iron accumulation, induces ferroptosis, and exacerbates secondary brain injury, while PIEZO1 dysfunction impairs cerebrovascular integrity and the blood-brain barrier. ③In traumatic brain injury, upregulation of PIEZO2 in neurons promotes neuronal death and pro-inflammatory cytokine release. ④Activation of PIEZO1 promotes fluid excretion in the brain, alleviating hydrocephalus. ⑤PIEZO1 dysfunction is involved in amyloid-beta toxicity, glial activation, vascular damage, and metabolic abnormalities in Alzheimer's disease. ⑥PIEZO1 activation inhibits myelination and modulates immune responses in multiple sclerosis. ⑦PIEZO1 mediates pulsatile pain characteristic of migraine induced by blood flow pulsation. ⑧Elevated intraocular pressure upregulates PIEZO1 and PIEZO2, leading to hyperexcitability and metabolic stress injury of retinal ganglion cells. ⑨PIEZO channels regulate neuronal excitability, proprioception, and baroreflex abnormalities in amyotrophic lateral sclerosis, and targeting PIEZO is a potential therapeutic strategy.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21692
BACKGROUND: Deep learning methods have made breakthrough progress in the field of bone imaging diagnosis. They have overcome the problems of easy misdiagnosis and low efficiency in traditional bone imaging diagnosis methods, and are conducive to the popularization of intelligent diagnosis methods in orthopedics. OBJECTIVE: To review the application, advantages and disadvantages of deep learning in the diagnosis of common bone diseases. METHODS: Literature published from January 2021 to June 2025 on deep learning-assisted skeletal image diagnosis was retrieved from CNKI, WanFang, PubMed, and Web of Science databases. Chinese and English search terms included “artificial intelligence, deep learning, machine learning, computer-aided diagnosis, skeletal imaging, fracture, bone tumor, osteoporosis, osteoarthritis, synovitis, spinal, cartilage, classification, detection, segmentation.” According to the inclusion criteria, 76 articles were finally included in this review. RESULTS AND CONCLUSION: Deep learning models have become powerful tools for bone imaging diagnosis and are gradually gaining recognition from clinicians, improving the efficiency of bone imaging diagnosis. Deep learning technology uses its image feature capture ability to help improve the clinical diagnosis of fractures, bone tumors, osteoporosis, osteoarthritis, synovitis, and spinal lesions, providing a reference for clinical decision-making. Although deep learning diagnostic applications have great potential, they are prone to insufficient model generalization and rely heavily on large amounts of annotated data, which reduces model credibility and hinders clinical translation. Future research should focus on improving the robustness and generalization of deep learning models. In summary, deep learning has certain reference value in clinical bone imaging diagnosis.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025124
Preeclampsia (PE) is a multisystem syndrome affecting 2–8% of pregnancies, with placental dysfunction as a central driver. Metabolic dysregulation, particularly aberrant glycolysis, has been implicated in PE pathogenesis, but the mechanistic links among glycolysis, protein lactylation, and pyroptosis remain undefined. This study combined bioinformatics analysis of PE-associated transcriptomes with experimental validation using placental tissues from PE patients and healthy controls. In vitro models employed hypoxic endothelial cell cultures, pharmacological glycolysis inhibition via 2-deoxyglucose, and genetic modulation of hexokinase 2 (HK2) through siRNA silencing and plasmid-based overexpression. Molecular profiling assessed key glycolytic enzymes, lactylation markers, and pyroptosis-related factors. PE placental tissues exhibited significantly higher expressions of glycolytic enzymes, elevated protein lactylation, and increased pyroptosis markers compared to controls. Hypoxic endothelial cells showed coordinated upregulation of these pathways. Pharmacological glycolysis inhibition significantly reduced lactylation and pyroptosis. HK2 silencing decreased glycolytic activity, attenuating lactylation and pyroptosis, while HK2 overexpression had opposite effects, underscoring its central regulatory role. These findings indicate that HK2-mediated glycolysis drives placental vascular endothelial lactylation and pyroptosis, revealing a novel mechanistic pathway in PE pathophysiology and identifying HK2 as a potential therapeutic target.