Stem Cell Research & Therapy•2026•DOI: 10.1186/s13287-026-05073-7
Exosomes have emerged as critical mediators of intercellular and inter-organ communication in bone biology. Secreted by bone-resident cells such as osteoblasts, osteoclasts, osteocytes, and mesenchymal stem cells (MSCs), these nanosized vesicles carry diverse molecular cargos that regulate bone remodeling, regeneration, and skeletal homeostasis. In addition to mediating local communication within the bone microenvironment, exosomes also participate in systemic crosstalk communication between bone and other tissues, including skeletal muscle, adipose tissue, gut microbiota, the immune system, the nervous system, and vasculature. Disruption of these exosome-mediated pathways contributes to the development and progression of bone diseases, including osteoporosis, osteoarthritis, osteonecrosis of the femoral head, and bone metastases. This review summarizes current advances in exosome-mediated signaling in both physiological and pathological contexts, with particular emphasis on their roles as biomarkers, therapeutic agents, and drug delivery vehicles. We also discuss the emerging contribution of artificial intelligence (AI) to exosome research, especially in biomarker discovery, disease classification, and target identification, as well as the major challenges that currently limit clinical translation. Together, these insights highlight the potential of exosome-based strategies for precision medicine in bone diseases.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026054
The anti-inflammatory properties of the traditional herb Salvia miltiorrhiza Bunge are well-established, yet its precise mechanism of action in ulcerative colitis (UC) remains unclear. Herein, we evaluate the therapeutic potential of four major tanshinones–tanshinone IIA (Tan IIA), miltirone, neocryptotanshinone, and dihydrotanshinone I–in a murine dextran sulfate sodium (DSS)-induced colitis model. Our results show that tanshinones effectively alleviate disease severity, suppress systemic and local inflammation, and restore intestinal barrier integrity. Integrated multi-omics analysis reveals that the therapeutic efficacy originates from a comprehensive reprogramming of the gut microbiota-metabolite axis. Specifically, tanshinones reverse colitis-associated dysbiosis and rectify metabolic disturbances in linoleic acid metabolism, bile acid biosynthesis, and amino acid utilization. Correlation network analysis identifies key functional modules linking beneficial microbes (e.g., Akkermansia) to anti-inflammatory lipid mediators and associating pathobionts (e.g., Desulfovibrio) with disrupted bile acid metabolism. Notably, supplementation with Akkermansia muciniphila synergizes with Tan IIA to amplify barrier restoration and metabolic normalization. Our findings establish that tanshinones ameliorate UC through microbiota-driven metabolic reprogramming, wherein the restructured microbial community actively shapes a therapeutic metabolic output. This work elucidates a metabolite-mediated mechanism of action and positions tanshinones as promising microbiome-targeting therapeutics for inflammatory bowel disease.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025170
Cryptococcus gattii causes cryptococcosis and life-threatening cryptococcal meningitis. Currently, the pathogenic virulence mechanisms of C. gattii remain a significant area of ongoing research with considerable unexplored aspects. On the basis of our established research, a sub-cluster of strains with independent evolutionary relationships from WM276 in the phylogenetic analysis of VGI-type strains is identified. In vivo infection experiments on this sub-branch of strains reveal that there are hypervirulent strains and hypovirulent strains among these strains, and the virulence differences are significant (P < 0.001). Bioinformatic interrogation of differentially expressed genes reveals that the catalase-encoding gene CGB_J0620W, CAT2, is a pivotal virulence-associated gene. The hypervirulent clinical isolate G4 (G4-WT) is selected as the parental strain, from which an isogenic CAT2-knockout mutant (cat2Δ) is constructed via homologous recombination, which shows increased sensitivity to oxidative stress, as well as growth defects in response to hyperosmosis, 5-fluorocytosine, fluconazole and amphotericin B. The cat2Δ::CAT2 strain exhibits phenotypic restoration to wild type (WT). In the mouse experiments, significant differences in survival (P < 0.001), pulmonary fungal burden (P < 0.01), and alveolar structural damage are observed between the WT and cat2Δ strains, which are completely different from C. neoformans. Moreover, comparative transcriptome analysis is performed on the WT and cat2Δ strains, which reveals that enzymes encoded by CAT2 may be involved in oxidative stress, metabolism and sugar transport. In conclusion, this study may explain the differences in virulence among different genetic evolutionary processes of a sub-cluster of the VGI geneotype of C. gattii and provide a theoretical basis for targeted therapy in a specific genotype population in the future.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026084
Osimertinib is the standard first-line treatment for patients with non-small cell lung cancer (NSCLC) harboring EGFR-sensitive mutations. However, drug resistance inevitably develops, highlighting the critical need for strategies to overcome this resistance and prolong therapeutic efficacy. Understanding the mechanisms underlying drug resistance is essential, and drug-resistant cell models serve as valuable tools for investigating acquired resistance. In this study, we establish an osimertinib resistance evolution model in vitro by continuous high-dose drug induction and identify cell lines exhibiting “permanent” resistance to osimertinib (osimertinib resistant, OR). Transcriptome sequencing (RNA-seq), gain- and loss-of-function assay, including lentiviral-mediated overexpression and RNAi knockdown, pharmacological inhibition, and protein degradation analysis reveal significant alterations in genes associated with epigenetic regulation, notably a marked upregulation of histone deacetylase 6 (HDAC6) in OR cells. Knockdown of HDAC6 or pharmacological inhibition of HDAC6 restores the sensitivity of OR cells to osimertinib, whereas overexpression of HDAC6 in sensitive cells reduces drug efficacy and accelerates the onset of resistance. Furthermore, we find that HDAC6 upregulation promotes EGFR degradation, thereby contributing to resistance. Collectively, our findings demonstrate the utility of drug resistance evolution models in identifying key resistance factors. HDAC6 plays a pivotal role in osimertinib resistance, and targeting HDAC6 may represent a novel therapeutic strategy to overcome resistance and enhance treatment efficacy.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024141
Diabetic nephropathy (DN) is recognized as one of the primary causes of chronic kidney disease and end-stage renal disease. Vaccarin (VAC) confers favorable effects on cardiovascular and metabolic diseases, including type 2 diabetes mellitus (T2DM). Nonetheless, the potential role and mechanism of VAC in the etiology of DN have yet to be completely elucidated. In this study, a classical mouse model of T2DM is experimentally induced via a high-fat diet (HFD)/streptozocin (STZ) regimen. Renal histological changes are assessed via H&E staining. Masson staining and immunohistochemistry (IHC) are employed to assess renal fibrosis. RT-PCR is utilized to quantify the mRNA levels of renal fibrosis, oxidative stress and inflammation markers. The levels of malondialdehyde (MDA) and reactive oxygen species (ROS), as well as the content of glutathione peroxidase (GSH-Px), are measured. The protein expressions of collagen I, TGF-β1, α-SMA, E-cadherin, Nrf2, catalase, SOD3, SOD2, SOD1, p-ERK, p-EGFR (Y845), p-EGFR (Y1173), p-NFκB P65, t-ERK, t-EGFR and t-NFκB P65 are detected by western blot analysis. Our results reveal that VAC has a beneficial effect on DN mice by improving renal function and mitigating histological damage. This is achieved through its inhibition of renal fibrosis, inflammatory cytokine overproduction, and ROS generation. Moreover, VAC treatment effectively suppresses the process of epithelial-mesenchymal transition (EMT), a crucial characteristic of renal fibrosis, in high glucose (HG)-induced HK-2 cells. Network pharmacology analysis and molecular docking identify epidermal growth factor receptor (EGFR) as a potential target for VAC. Amino acid site mutations reveal that Lys-879, Ile-918, and Ala-920 of EGFR may mediate the direct binding of VAC to EGFR. In support of these findings, VAC reduces the phosphorylation levels of both EGFR and its downstream mediator, extracellular signal-regulated kinase 1/2 (ERK1/2), in diabetic kidneys and HG-treated HK-2 cells. Notably, blocking either EGFR or ERK1/2 yields renal benefits similar to those observed with VAC treatment. Therefore, this study reveals that VAC attenuates renal damage via inactivation of the EGFR/ERK1/2 signaling axis in T2DM patients.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024149
Nonalcoholic fatty liver disease (NAFLD) is a leading cause of chronic liver disease and poses a substantial health burden with increasing incidence globally. NAFLD encompasses a spectrum extending from hepatic steatosis to nonalcoholic steatohepatitis (NASH), with the possibility of progressing to cirrhosis or, in severe instances, hepatocellular carcinoma (HCC). NAFLD extends beyond simple metabolic disruption and involves multiple immune cell-mediated inflammatory processes. Integrins are a family of heterodimeric transmembrane cell adhesion receptors that regulate various aspects of NAFLD onset and progression, including hepatocellular steatosis, hepatic stellate cell (HSC) activation and immune cell infiltration. In this review, we comprehensively summarize the involvement of integrins in NAFLD, as well as the downstream signal transduction mediated by these receptors. Furthermore, we present the latest clinical and preclinical findings on drugs that target integrins for steatosis, inflammation, fibrosis and NAFLD-related HCC treatment.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2024245
Amycolatopsis mediterranei U32 is an industrial strain capable of producing therapeutically useful rifamycin SV. In early days of fermentation studies, nitrate was found to increase the yield of rifamycin along with globally, affecting both carbon and nitrogen metabolism in favor of antibiotic biosynthesis; thus, the nitrate-stimulating effect (NSE) hypothesis was proposed. Although GlnR is likely the master regulator of the pleotropic effect of NSE, the global metabolism affected by NSE has never been systematically examined. In this study, we use mass spectrometry-based metabolomics to quantitatively monitor the metabolomic responses of A. mediterranei U32 to nitrate supplementation. The concentrations of many metabolites involved in central carbon metabolism, including glucose 6-phosphate, glucose 1-phosphate, UDP-glucose, and acetyl-coenzyme A, decrease significantly after the addition of 80 mM potassium nitrate to the medium. We find that the rifamycin SV production yield could be increased by the addition of glucose during the logarithmic growth phase. Moreover, at multiple time points during glucose supplementation in the mid- and late-exponential phases, the yield of rifamycin SV further increases, reaching 354.3%. Quantitative real-time PCR assays of the key genes corresponding to the synthesis of the rifamycin SV precursor combined with data from metabolomics analysis confirm that carbon source deficiency is compensated for after glucose supplementation and that the expression of genes involved in the pathway of 3-amino-5-hydroxybenzoic acid synthesis by UDP-glucose and glutamine is significantly increased. This preliminary exploration of dynamic metabolomic profiles has the potential to increase our understanding of the NSE.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024188
DNA replication stress is a significant contributor to spontaneous DNA damage and genome instability. While the impact of p53 deficiency on increasing DNA replication stress is known, the specific molecular mechanism underlying this phenomenon remains poorly understood. This study explores how p53 deficiency induces DNA replication stress by activating mTORC1 through R-loop formation, which is facilitated by the upregulation of RNR. Research has shown that p53 deficiency results in increased γH2AX expression and a higher mutation rate in the HPRT gene. Interestingly, these effects can be alleviated by rapamycin, an mTORC1 inhibitor. Additionally, rapamycin reduces the abundance of R-loop structures in p53KO cells, which is linked to mTORC1’s regulation of ribonucleotide reductase (RNR) level. These findings suggest that p53 deficiency-induced DNA replication stress relies on mTORC1 activation, with the upregulation of RNR expression and R-loop formation. Overall, this study underscores the importance of R-loops in mTORC1 activation-dependent DNA replication stress triggered by p53 deficiency.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024048
Bone cancer pain (BCP), due to cancer bone metastasis and bone destruction, is a common symptom of tumors, including breast, prostate, and lung tumors. Patients often experience severe pain without effective treatment. Here, using a mouse model of bone cancer, we report that MOTS-c, a novel mitochondrial-derived peptide, confers remarkable protection against cancer pain and bone destruction. Briefly, we find that the plasma level of endogenous MOTS-c is significantly lower in the BCP group than in the sham group. Accordingly, intraperitoneal administration of MOTS-c robustly attenuates bone cancer-induced pain. These effects are blocked by compound C, an AMPK inhibitor. Furthermore, MOTS-c treatment significantly enhances AMPKα1/2 phosphorylation. Interestingly, mechanical studies indicate that at the spinal cord level, MOTS-c relieves pain by restoring mitochondrial biogenesis, suppressing microglial activation, and decreasing the production of inflammatory factors, which directly contribute to neuronal modulation. However, in the periphery, MOTS-c protects against local bone destruction by modulating osteoclast and immune cell function in the tumor microenvironment, providing long-term relief from cancer pain. Additionally, we find that chronic administration of MOTS-c has little effect on liver, renal, lipid or cardiac function in mice. In conclusion, MOTS-c improves BCP through peripheral and central synergistic effects on nociceptors, immune cells, and osteoclasts, providing a pharmacological and biological rationale for the development of mitochondrial peptide-based therapeutic agents for cancer-induced pain.
Chinese Traditional and Herbal Drugs•2026•DOI: 10.7501/j.issn.0253-2670.2026.15.20261512
Casticin, a polymethoxyflavone derived from Vitex trifolia, was evaluated for its therapeutic efficacy and mechanism in colitis-associated colorectal cancer (CAC) using an azoxymethane/dextran sulfate sodium (AOM/DSS) mouse model. Casticin intervention significantly attenuated body weight loss, reduced disease activity index, and decreased colonic tumor volume and tumor burden (P < 0.05), while improving survival rates of tumor-bearing mice. Safety assessments revealed no significant abnormalities in serum liver function indicators or major organ histomorphology. 16S rRNA sequencing demonstrated that casticin reversed CAC-induced gut dysbiosis, notably downregulating the pro-carcinogenic phyla Fusobacteriota and Patescibacteria, and enriching anti-inflammatory short-chain fatty acid-producing genera Lachnospiraceae_NK4A136_group and Prevotellaceae_UCG-001. Proteomic profiling identified the complement and coagulation cascades as the core responsive pathway, with dose-dependent restoration of serine protease inhibitor 1 (Serpine1) and integrin alpha M (Itgam) expression. Western blotting confirmed significant downregulation of Itgam and Serpine1 in colonic tissue (P < 0.01 and P < 0.001, respectively), consistent with proteomic trends. Correlation analysis further revealed that beneficial genera such as Lachnospiraceae_NK4A136_group were negatively correlated with Serpine1 expression, whereas pro-carcinogenic Fusobacteriota was positively correlated with Itgam expression. These findings indicate that casticin ameliorates CAC by remodeling gut microbiota composition and modulating key molecules in the complement and coagulation cascades, thereby synergistically blocking the inflammation-to-cancer transition.
Stem Cell Research & Therapy•2026•DOI: 10.1186/s13287-026-05073-7
Exosomes have emerged as critical mediators of intercellular and inter-organ communication in bone biology. Secreted by bone-resident cells such as osteoblasts, osteoclasts, osteocytes, and mesenchymal stem cells (MSCs), these nanosized vesicles carry diverse molecular cargos that regulate bone remodeling, regeneration, and skeletal homeostasis. In addition to mediating local communication within the bone microenvironment, exosomes also participate in systemic crosstalk between bone and other tissues, including skeletal muscle, adipose tissue, gut microbiota, the immune system, the nervous system, and vasculature. Disruption of these exosome-mediated pathways contributes to the development and progression of bone diseases, including osteoporosis, osteoarthritis, osteonecrosis of the femoral head, and bone metastases. This review summarizes current advances in exosome-mediated signaling in both physiological and pathological contexts, with particular emphasis on their roles as biomarkers, therapeutic agents, and drug delivery vehicles. We also discuss the emerging contribution of artificial intelligence (AI) to exosome research, especially in biomarker discovery, disease classification, and target identification, as well as the major challenges that currently limit clinical translation. Together, these insights highlight the potential of exosome-based strategies for precision medicine in bone diseases.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026054
The anti-inflammatory properties of the traditional herb Salvia miltiorrhiza Bunge are well-established, yet its precise mechanism of action in ulcerative colitis (UC) remains unclear. Herein, we evaluate the therapeutic potential of four major tanshinones–tanshinone IIA (Tan IIA), miltirone, neocryptotanshinone, and dihydrotanshinone I–in a murine dextran sulfate sodium (DSS)-induced colitis model. Our results show that tanshinones effectively alleviate disease severity, suppress systemic and local inflammation, and restore intestinal barrier integrity. Integrated multi-omics analysis reveals that the therapeutic efficacy originates from a comprehensive reprogramming of the gut microbiota-metabolite axis. Specifically, tanshinones reverse colitis-associated dysbiosis and rectify metabolic disturbances in linoleic acid metabolism, bile acid biosynthesis, and amino acid utilization. Correlation network analysis identifies key functional modules linking beneficial microbes (e.g., Akkermansia) to anti-inflammatory lipid mediators and associating pathobionts (e.g., Desulfovibrio) with disrupted bile acid metabolism. Notably, supplementation with Akkermansia muciniphila synergizes with Tan IIA to amplify barrier restoration and metabolic normalization. Our findings establish that tanshinones ameliorate UC through microbiota-driven metabolic reprogramming, wherein the restructured microbial community actively shapes a therapeutic metabolic output. This work elucidates a metabolite-mediated mechanism of action and positions tanshinones as promising microbiome-targeting therapeutics for inflammatory bowel disease.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026084
Osimertinib is the standard first-line treatment for patients with non-small cell lung cancer (NSCLC) harboring EGFR-sensitive mutations. However, drug resistance inevitably develops, highlighting the critical need for strategies to overcome this resistance and prolong therapeutic efficacy. Understanding the mechanisms underlying drug resistance is essential, and drug-resistant cell models serve as valuable tools for investigating acquired resistance. In this study, we establish an osimertinib resistance evolution model in vitro by continuous high-dose drug induction and identify cell lines exhibiting “permanent” resistance to osimertinib (osimertinib resistant, OR). Transcriptome sequencing (RNA-seq), gain- and loss-of-function assay, including lentiviral-mediated overexpression and RNAi knockdown, pharmacological inhibition, and protein degradation analysis reveal significant alterations in genes associated with epigenetic regulation, notably a marked upregulation of histone deacetylase 6 (HDAC6) in OR cells. Knockdown of HDAC6 or pharmacological inhibition of HDAC6 restores the sensitivity of OR cells to osimertinib, whereas overexpression of HDAC6 in sensitive cells reduces drug efficacy and accelerates the onset of resistance. Furthermore, we find that HDAC6 upregulation promotes EGFR degradation, thereby contributing to resistance. Collectively, our findings demonstrate the utility of drug resistance evolution models in identifying key resistance factors. HDAC6 plays a pivotal role in osimertinib resistance, and targeting HDAC6 may represent a novel therapeutic strategy to overcome resistance and enhance treatment efficacy.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21247
BACKGROUND: Mitophagy plays a crucial regulatory role in the occurrence and development of cardiovascular diseases. Exercise intervention can mediate mitophagy to improve cardiovascular function, which provides new insights for the clinical prevention and treatment of cardiovascular diseases. OBJECTIVE: To summarize the regulatory role of mitophagy in cardiovascular diseases, the influence of exercise on mitophagy, and the mechanism by which exercise-mediated mitophagy improves cardiovascular diseases. METHODS: PubMed and CNKI databases were searched for relevant literature using the search terms of “mitophagy, mitochondrial function, cardiovascular disease, aerobic exercise, resistance training, combined aerobic resistance exercise, high-intensity interval training” in Chinese and English, respectively. Based on the inclusion and exclusion criteria, totally 88 documents were finally included for summary and analysis. RESULTS AND CONCLUSION: (1) Mitophagy plays a crucial role in the regulation of cardiovascular diseases such as heart failure, myocardial hypertrophy, atherosclerosis, and myocardial ischemia-reperfusion injury. Moreover, mitophagy imbalance or disorder can exacerbate the pathological process of cardiovascular diseases. (2) Various exercise modalities can activate mitophagy by regulating the expression of mitophagy-related factors. Among them, aerobic exercise can promote the formation of autophagosomes, thereby enhancing the regulation of mitophagy; resistance exercise can regulate mitochondrial biogenesis; combined aerobic and resistance exercise can further influence mitophagy by promoting lysosomal biogenesis; high-intensity interval training enhances mitophagy function by regulating the expression of mitochondrial dynamics-related proteins. (3) Exercise regulates mitophagy to alleviate myocardial fibrosis, inhibit cardiomyocyte apoptosis, regulate myocardial oxidative stress, and improve endothelial cell function, thereby playing a key role in the prevention and treatment of cardiovascular diseases, providing a new perspective for exercise promoting health and preventing cardiovascular diseases.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21259
BACKGROUND: Thyroid hormones play a critical role in regulating growth, development, energy metabolism, and maintaining homeostasis in mammals. Exercise interventions can modulate thyroid hormones levels through various mechanisms. However, the regulatory effects of exercise on multiple organs via thyroid hormones have not yet been fully elucidated. OBJECTIVE: To summarize thyroid hormones synthesis, metabolism, and its regulation through exercise, and explore its dynamic regulatory functions in the liver, bone, muscle, heart, and brain. METHODS: A comprehensive search was conducted in databases including China National Knowledge Infrastructure (CNKI), WanFang database, VIP, Web of Science, and PubMed for relevant articles published from database inception until February 2025. The search terms were “thyroid hormones, thyroxine, triiodothyronine, thyroid, hypothyroidism, hyperthyroidism, exercise, training, physical activity, liver, hepatic, muscle, bone, osteoporosis, osteoblasts, osteoclasts, heart, myocardium, cardiomyopathy, cardiac, myocardial infarction, brain, cognition, nervous” in Chinese and English. A total of 81 studies were included in this review. RESULTS AND CONCLUSION: Exercise can regulate thyroid hormones levels, reshape tissue-specific expression of deiodinases, or alter target organ thyroid hormone receptor sensitivity, forming dynamic regulation of multiple organs. Exercise interventions have the potential to reverse multi-organ pathological phenotypes caused by thyroid dysfunction, such as metabolic dysfunction-associated fatty liver disease, bone homeostasis imbalance, muscle function decline, cardiac function decline, and cognitive dysfunction. Although existing evidence reveals the regulatory effects of exercise on thyroid hormones, its molecular mechanisms and regulatory effects on multiple organs still need further analysis. In addition, current related studies are mostly based on rodents and mostly aerobic exercise; the extent to which they apply to human metabolic diseases requires more clinical evidence support.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21420
BACKGROUND: Surgical decision-making for posterior cruciate ligament avulsion fractures is highly dependent on imaging evaluation. Traditional methods rely on subjective interpretation of CT images, which suffer from limitations such as difficulties in quantifying three-dimensional spatial displacement parameters and insufficient precision in assessing rotational angles. Given the advancements in artificial intelligence (AI) technology, there is a need to develop automated, intelligent image recognition software based on AI algorithms. OBJECTIVE: To investigate the intelligent diagnostic capabilities of AI algorithms for posterior cruciate ligament tibial avulsion fractures in 3D CT images and their effectiveness in accurately assessing 3D parameters of fracture fragments. METHODS: Knee CT data from 24 patients with posterior cruciate ligament tibial avulsion fractures who were treated at the Wangjing Hospital of the China Academy of Chinese Medical Sciences between December 1, 2022, and August 30, 2024, were retrospectively collected. Three-dimensional reconstruction, intelligent fracture point recognition, and simulated reduction were performed using self-developed AI image recognition software. Translational and rotational parameters of the fracture fragments along the X, Y, and Z axes were obtained. These measurements were compared with those from traditional radiology reading software (PACS system) using rank-sum tests, Bland-Altman analysis, and linear regression models to assess consistency, and coefficients of variation were calculated to verify software stability. RESULTS AND CONCLUSION: ①There were no significant differences between AI software and traditional methods in measuring fracture fragment displacement (X/Y/Z axis translation and rotation) (P > 0.05). ②Bland-Altman analysis showed good consistency between the two methods, with no significant differences (P > 0.05). ③Linear regression models for X, Y, Z axis displacement and angles showed R² values > 0.99. ④The coefficients of variation for three repeated fracture point identifications by the AI software showed that for total fracture identification, 21 cases had coefficients of variation < 20%, and for articular surface fracture points, 18 cases had coefficients of variation < 20%. ⑤These findings indicate that the AI image recognition software can accurately quantify three-dimensional parameters of posterior cruciate ligament avulsion fracture fragments, with measurement results consistent with traditional methods and good stability. It can assist doctors in judging the degree of displacement and provide precise data support for preoperative planning. The software has good application prospects in avulsion fractures, and future studies should expand the sample size and further verify its impact on surgical outcomes.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21322
BACKGROUND: Research on the mechanical stability imbalance mechanism in intervertebral disc degeneration has long focused on the paraspinal muscles, with insufficient attention paid to the anterior/posterior abdominal wall and hip core muscle groups. There is a particular lack of systematic analysis of the synergistic actions of multiple muscle groups, and the link between molecular mechanisms and muscle function remains unclear. OBJECTIVE: To integrate evidence on the association between the anterior/posterior abdominal wall, paraspinal, and hip core muscle groups and intervertebral disc degeneration, to elucidate interaction of synergistic muscle imbalance with molecular pathways such as Piezo1–YAP, and to propose targeted prevention and treatment strategies. METHODS: A search was conducted in CNKI, WanFang, PubMed and Web of Science using a combination of MeSH terms (e.g., transversus abdominis[MeSH]) and free terms (e.g., TrA, IVDD) connected by Boolean operators (AND/OR) for muscle anatomy terms (transversus abdominis, gluteus maximus, etc.), disease terms (intervertebral disc degeneration, low back pain, etc.), and study types (RCT, cohort study, etc.). Finally, 61 articles were selected according to preset criteria for analysis. RESULTS AND CONCLUSION: There is a complex association between lumbar core muscles and intervertebral disc degeneration. The transversus abdominis maintains lumbar stability by regulating intra-abdominal pressure and thoracolumbar fascia tension; its decompensation (inhibition/atrophy) is an important pathological feature of intervertebral disc degeneration. Meanwhile, patients with intervertebral disc degeneration exhibit characteristic synergistic dysfunction of core muscles: (1) antagonistic compensation of abdominal wall muscles (overactivation of internal/external oblique to compensate for transversus abdominis dysfunction); (2) dual compensation in the quadratus lumborum region (intra-regional psoas-quadratus lumborum synergistic reorganization, inter-regional erector spinae-quadratus lumborum/psoas compensation); (3) gluteal muscle imbalance (gluteus maximus fatty infiltration/inhibition, gluteus medius protective compensation on the dominant side). These synergistic dysfunctions are core links in disrupting spinal stability and accelerating intervertebral disc degeneration. Multi-muscle synergistic imbalance (e.g., disruption of the gluteus-psoas-abdominal muscle kinetic chain) not only exacerbates local mechanical abnormalities but also affects overall spine-pelvic biomechanical balance through systemic compensation, and causes dysregulation of intra-abdominal pressure. Molecular mechanism studies indicate that abnormal mechanical loading activates the Piezo1-Ca²⁺-F-actin-YAP signaling axis, promoting extracellular matrix degradation and inflammatory responses; meanwhile, imbalance of the nuclear factor E2-related factor 2/nuclear factor κB pathway exacerbates oxidative stress and inflammatory microenvironment, forming a mechanical-biological vicious cycle. Intervention strategies targeting recovery of core muscle synergistic function (e.g., transversus abdominis targeted training, gluteal strengthening, correction of abnormal activation patterns) and their combination with molecular targeted drugs have important clinical potential. Future research should delve into the mechanisms of interaction among muscle groups and compensation patterns to optimize prevention and treatment strategies for intervertebral disc degeneration.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21558
BACKGROUND: Oxidative stress induced by chronic hyperglycemia and impaired antioxidant systems are one of the core mechanisms underlying the onset and progression of diabetes mellitus. Ferroptosis, a new type of programmed cell death caused by iron-dependent lipid peroxidation, has received considerable academic interest due to its association with diabetes. OBJECTIVE: To reveal the current status and trends of ferroptosis-related research in the field of diabetes mellitus using bibliometric methods, aiming to offer academic resources to further develop this research area. METHODS: Based on the Web of Science Core Collection database, with a time span set from January 1, 2015 to January 1, 2025, 797 articles related to ferroptosis in the field of diabetes were retrieved. After deduplication, 758 high-quality articles were analyzed using CiteSpace (6.2.R1) for visualization of publication output, country/institution collaboration, high-impact authors/reference co-citation, keyword co-occurrence/clustering/burst detection, and international frontier trends. RESULTS AND CONCLUSION: Bibliometric analysis showed a substantial growth in ferroptosis-related research in diabetes. Among the 758 records, Linkermann, Andreas was the most prolific author, while Dixon SJ established an academic influence benchmark with 420 citations. The journal Cell served as a key knowledge dissemination hub. The most frequent keywords included oxidative stress, cell death, and lipid peroxidation, with clusters mainly focusing on diabetic nephropathy and cardiomyopathy, glutathione peroxidase 4, and necroptosis. The application of ferroptosis regulatory networks is deepening and has become an emerging paradigm for targeted therapy research in diabetes and its complications.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026033
Metabolic dysfunction-associated steatohepatitis (MASH) has become a global epidemic, and effective therapeutic strategies are urgently needed. Lonidamine (LND) has been reported to possess anti-inflammatory effects; however, few studies have investigated whether LND exerts a therapeutic effect on MASH. Therefore, in this study, we aim to explore the effects of LND on inflammatory responses and abnormal lipid metabolism in MASH mice. A mouse MASH model is established by feeding C57BL/6 mice a high-fat, high-cholesterol (CL) diet. The results show that LND attenuates CL-induced increases in body weight, serum glucose and lipid levels, inflammatory responses, and hepatocellular steatosis. In addition, the mitogen-activated protein kinase (MAPK) signaling pathway is inhibited, and the expression level of sterol regulatory element-binding protein 1 (SREBP1) protein is significantly reduced. Meanwhile, in vitro models of cellular inflammation and lipid metabolism are simulated, and molecular docking and biolayer interferometry (BLI) analysis are used to verify that LND and SREBP1 have a direct interaction and that LND promotes the degradation of SREBP1. Furthermore, specific knockdown of Srebp1 in AML12 cells is performed to further verify the effect of LND on MASH. The results confirm that LND exerts anti-inflammatory effects in MASH by inhibiting the activity of the MAPK signaling pathway and improves abnormal lipid metabolism through its interaction with SREBP1. Overall, LND holds promise as a potential therapeutic agent for the treatment of MASH.