Chinese Journal of New Drugs•2025•DOI: 10.1007/s12613-024-1234-5
The dissolution behavior of vanadium slag in the process of vanadium extraction using the calcium roasting–acid leaching method was systematically investigated. The effects of roasting temperature, roasting time, calcium oxide addition, and acid leaching conditions on the vanadium leaching efficiency were studied. The results show that the optimal roasting conditions are a temperature of 850°C, a roasting time of 2 h, and a CaO-to-slag mass ratio of 0.3. Under these conditions, a vanadium leaching efficiency of 92.5% can be achieved. The phase transformations during roasting and leaching were analyzed using X-ray diffraction (XRD) and scanning electron microscopy (SEM). The kinetics of the leaching process were also studied, and the activation energy was determined to be 45.2 kJ/mol. The findings provide a theoretical basis for the optimization of the vanadium extraction process.
Stem Cell Research & Therapy•2026•DOI: 10.1186/s13287-026-05026-0
Background Osteonecrosis of the femoral head (ONFH) is a progressive orthopedic disorder that often culminates in femoral head collapse and joint failure. Dysfunction of bone marrow mesenchymal stem cells (BMSCs), including impaired osteogenesis, enhanced adipogenesis, and mitochondrial dysfunction, has been increasingly recognized as a central driver of ONFH pathogenesis. However, the molecular mechanisms linking metabolic stress to lineage imbalance remain poorly defined.
Methods Paired BMSCs were isolated from necrotic femoral head regions (fhBMSCs) and the iliac crest (iBMSCs) of ONFH patients. Functional assays, RNA sequencing, and molecular analyses were performed to evaluate the effects of the hypoxia mimetic dimethyloxalylglycine (DMOG) on osteogenic–adipogenic balance, mitochondrial function, and senescence. Loss-of-function experiments targeting hypoxia-inducible factor-1α (HIF-1α) and Homer3 were conducted to elucidate mechanistic pathways.
Results Compared with iBMSCs, fhBMSCs exhibited impaired osteogenesis, enhanced adipogenesis, mitochondrial dysfunction, and increased senescence. DMOG pretreatment restored osteogenic differentiation, suppressed adipogenesis, improved mitochondrial dynamics, reduced oxidative stress, and enhanced bioenergetic metabolism. These protective effects were dependent on HIF-1α stabilization. Transcriptomic profiling identified Homer3 as a downstream negative regulator of HIF-1α. Homer3 was aberrantly upregulated in fhBMSCs but suppressed by DMOG, and its knockdown mimicked the effects of DMOG by promoting osteogenesis, inhibiting adipogenesis, enhancing mitophagy, and restoring mitochondrial function. Conversely, silencing HIF-1α abolished DMOG-mediated benefits and reinstated Homer3 expression.
Stem Cell Research & Therapy•2025•DOI: 10.1186/s13287-025-04504-1
Background It is well established that the mesenchymal stromal cell (MSC) therapeutic potency can be enhanced by cytokine pre-activation or licensing. However, its effects on therapeutic efficacy of small extracellular vesicles (MSC-sEV) have not yet been well established. Here we report on two different cytokine licensing strategies, using either a pro-inflammatory or anti-inflammatory cytokine and evaluate their therapeutic potency in vitro and in a preclinical model of corneal chemical burn. Methods BALB/c MSCs were cultured with no supplement, recombinant IFNγ, or recombinant TGFβ1 for 72 h. sEV, sEVIFNγ, and sEVTGFβ were then isolated from conditioned medium of parental cells by a combination of ultrafiltration and size exclusion chromatography. Following isolation MSC-sEV were thoroughly characterized for size, marker expression and therapeutic efficacy. To evaluate their immunomodulatory capacity, both naïve and licensed MSC-sEV were tested in in vitro macrophage and T cell assays and in a preclinical corneal injury model. Results Relative to unlicensed sEV, sEVIFNγ exhibited increased expression of MHC I and PD-L1 on their surface, whereas sEVTGFβ expressed higher levels of CD44, CD29, and CD73. For immunomodulatory capacity, only sEVTGFβ was found to reduce macrophage expression of MHC II and CD80 and induced the secretion of anti-inflammatory macrophage cytokines. sEVTGFβ were also found to increase Treg expansion and FOXP3 expression. Given the superior efficacy observed of sEVTGFβ in vitro, this product was evaluated in a preclinical mouse model of corneal chemical burn. sEVTGFβ were applied either topically (day 0, 1, and 3) or subconjunctivally (day 0, and 3), and mice were monitored for 14 days. sEVTGFβ ameliorated burn-induced structural damage and accelerated restoration of normal corneal thickness, compared to PBS-treated controls. sEVTGFβ also resulted in reduced inflammatory mediators (IL-1β, iNOS) and minimised levels of fibrosis-associated collagen in the cornea. Mice that received subconjunctival, but not topical, administration of sEVTGFβ exhibited regulatory immune cell profiles with reduced pro-inflammatory-
Stem Cell Research & Therapy•2025•DOI: 10.1186/s13287-025-04229-1
Background Despite numerous studies addressing the molecular mechanisms by which pluripotent stem cells (PSCs) maintain self-renewal and pluripotency under normal culture conditions, the fundamental question of how PSCs manage to survive stressful conditions remains largely unresolved. Post-transcriptional/translational regulation emerges to be vital for PSCs, but how PSCs coordinate and balance their survival and differentiation at translational level under extrinsic and intrinsic stress conditions is unclear. Methods The high-throughput sequencing of cross-linking immunoprecipitation cDNA library (HITS-CLIP) was employed to decipher the genome-wide OCT4-RNA interactome in human PSCs, a combined RNC-seq/RNA-seq analysis to assess the role of OCT4 in translational regulation of hypoxic PSCs, and an OCT4-protein interactome to search for OCT4 binding partners that regulate cap-independent translation initiation. By taking the Heterozygous Knocking In N-terminal Tags (HKINT) approach that specifically disrupts the 5'-UTR secondary structure and tagging its protein product of the mRNA from one allele while leaving that from the other allele intact, we examined the effect of disrupting the OCT4/5'-UTR interaction on translation of AKT1 mRNA. Results We revealed OCT4 as a bona fide RNA-binding protein (RBP) in human PSCs that bound to the 5'-UTR, 3'-UTR and CDS regions of mRNAs. Multiple known proteins participating in IRES-mediated translation initiation were detected in the OCT4-protein interactome, and a combined RNC-seq/RNA-seq analysis further confirmed a crucial role of OCT4 in translational regulation of PSCs in response to hypoxic stress. Remarkably, OCT4 bound to the GC-rich elements in the 5'-UTR of AKT1 and multiple PI3K/AKT-pathway-gene mRNAs, and promoted their translation initiation via IRES-mediated pathways under stress conditions. Specifically disrupting the AKT1 mRNA 5'-UTR structure and the OCT4/5'-UTR interaction by the HKINT approach significantly reduced the translation level of AKT1 that led to a higher susceptibility of PSCs to oxidative stress-induced apoptotic death and prioritized differentiation toward ectoderm and endoderm. Conclusions Our results reveal OCT4 as an anti-stress RBP for translational regulation that critically coordinates the survival and differentiation of PSCs in response to various stressors.
Stem Cell Research & Therapy•2024•DOI: 10.1186/s13287-024-03838-6
Correction to: Stem Cell Research & Therapy (2023) 14:17. The authors note that during the preparation of the manuscript, the track plot included the expression trends of 14 genes (with Tk1 and Pclaf repeated twice), but only 13 gene symbols were labeled, resulting in a mismatch and repeat of the trackplot with the image on the right. This error occurred during the typesetting process of the original figures. The authors have corrected the annotations in Fig. 2C as shown ahead in this correction article, apologise for the error, and confirm that the overall results and conclusions are not affected by this change.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025148
Mesothelial cells play an important role in colorectal cancer peritoneal metastasis (CRC-PM), where they support tumor growth and invasion. In this study, we investigate the molecular mechanisms by which mesothelial cells contribute to CRC metastasis. Using single-cell RNA sequencing (scRNA-seq) on tissue samples from 12 CRC patients with peritoneal metastasis, we identify PDK4 as a key gene in mesothelial cells during metastasis. The expression of PDK4 is significantly greater in mesothelial cells undergoing mesothelial-to-mesenchymal transition (MMT) compared to normal peritoneal cells, suggesting its involvement in mesothelial cell reprogramming during peritoneal metastasis. In vitro experiments show that coculturing mesothelial cells with CRC cells leads to increased PDK4 expression, which in turn enhances mesothelial cell migration and invasion. Knockdown of PDK4 reduces mesothelial cell invasion, while overexpression of PDK4 increases invasive ability, highlighting its critical role in mesothelial cell invasion. Additionally, PDK4 promotes metabolic changes, specifically increasing fatty acid oxidation (FAO), which is necessary for mesothelial cell invasion. Blocking FAO reduces the invasive ability of PDK4-overexpressing mesothelial cells, while restoring FAO in PDK4-knockdown cells rescues their invasion potential. Further analysis shows that PDK4 enhances the acetylation of β-catenin, a protein involved in cell movement, and that this modification is crucial for mesothelial cell invasion. Our results suggest that PDK4 regulates mesothelial cell invasion through β-catenin acetylation following metabolic reprogramming, offering a potential target for therapies aimed at inhibiting CRC-PM.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025005
Pulpitis is a common inflammatory oral disease that can lead to pulp necrosis. The aim of this study is to investigate the expression and regulatory mechanisms of ATF3, a potential therapeutic marker, in pulpitis. A mouse pulpitis model with different degrees of inflammation is established, and the expression of ATF3 in pulpitis is explored. The histological features of healthy pulp and pulpitis are analyzed by HE staining, and classical inflammatory factors are detected by immunohistochemistry (IHC). In an in vitro study, we investigate the role of ATF3 in the regulation of WNT4 transcription and explore the effects of the ATF3/WNT4 axis on the polarization of RAW264.7 macrophages, the inflammatory response and the osteogenic differentiation of human dental pulp stem/stromal cells (hDPSCs). Our results show that ATF3 is expressed at low levels in inflamed pulp tissues; overexpression of ATF3 reduces the area of pulp necrosis, decreases the level of pro-inflammatory factors, and promotes macrophage polarization toward the M2 type. Furthermore, we reveal that ATF3 binds to the WNT4 promoter region and positively regulates the expression of WNT4 and that ATF3 downregulates M1 markers and increases the expression of M2 markers by regulating WNT4 expression. In addition, ATF3 promotes the osteogenic differentiation of dental pulp stem cells. In summary, this study reveals that ATF3 promotes M2 macrophage polarization by regulating WNT4, which in turn inhibits pulpal inflammatory responses and promotes the osteogenic differentiation of dental pulp stem cells. These findings suggest that ATF3 may be a potential target for pulpitis treatment.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025231
The intestinal microbiota plays critical roles in regulating immunity and inflammation through intricate interactions between microbial metabolites and diverse immune cells. Dendritic cells (DCs), the most potent professional antigen-presenting cells, are essential for sensing the complicated microbiota environment and subsequently initiating and regulating adaptive immune responses. While the commensal microbiota typically mediates DC-triggered immune tolerance and thus the maintenance of intestinal homeostasis, epithelial injury or pathogenic infection generally drives the proinflammatory function of DCs, contributing to harmful inflammation and intestinal disorders. Various microbiota metabolites (such as short-chain fatty acids, bile acids, and tryptophan derivatives) play critical roles in modulating the developmental and functional diversity of DCs through metabolic, epigenetic, or signaling reprogramming. In this review, we discuss the metabolic crosstalk between the intestinal microbiota and DCs and its pivotal function in orchestrating the balance between intestinal homeostasis and pathogenic inflammation. We also discuss future directions to better elucidate the microbiota-DC dialog in intestinal immunity and develop therapeutic approaches for manipulating the microbiota-DC axis against inflammatory disorders.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025158
Kinesin family member 14 (KIF14) has been implicated in the progression of multiple cancer types, yet its role in colorectal cancer (CRC) metastasis remains undefined. Here, we assesse KIF14 expression in CRC specimens and explore its clinical and functional significance. KIF14 upregulation is frequently observed in CRC tissues and is correlated with advanced tumor stage and reduced overall survival. Functional assays reveal that KIF14 depletion in CRC cells inhibits migration, invasion, and in vivo metastatic colonization, whereas KIF14 overexpression induces the opposite effects. Transcriptomic and pathway enrichment analyses reveal that KIF14 functions as a critical regulator of focal adhesion and cell-matrix adhesion signaling. This finding is further supported by experimental evidence showing that KIF14 overexpression promotes focal adhesion assembly, whereas KIF14 knockdown disruptes this process. Mechanistically, we demonstrate that KIF14 binds directly to the focal adhesion protein vinculin and mediates its delivery to the leading edge of migrating cells. Moreover, bioinformatics prediction and chromatin immunoprecipitation confirm that E2F1 directly binds the KIF14 promoter to drive its transcription. Rescue experiments reveal that ectopic KIF14 expression restores the prometastatic phenotypes suppressed by E2F1 silencing, indicating that the effects of E2F1 are mediated by the E2F1-KIF14 axis. Collectively, our findings reveal a novel E2F1-KIF14-vinculin signaling axis that drives CRC metastasis by modulating focal adhesion dynamics, highlighting KIF14 as a potential therapeutic target.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2024168
Uncoupling protein-2 (UCP2) controls the antioxidant response and redox homeostasis in cancer and is considered a potent molecular target for cancer treatment. However, the specific mechanism of UCP2 inhibition and its role in glioblastoma (GBM) have not yet been elucidated. Here, we attempt to identify a UCP2 inhibitor and study the underlying molecular mechanism in GBM. Bioinformatics analysis and immunohistochemistry are used to validate the high expression of UCP2 in GBM and its prognostic significance. Drug intervention and tumor xenograft experiments are conducted to determine the inhibitory effect of genipin, a UCP2 inhibitor, on UCP2. The mitochondrial membrane potential and key ferroptosis genes are examined to determine the occurrence of ferroptosis. High expression of UCP2 in GBM is associated with poor prognosis, and inhibiting UCP2 can alleviate the malignant behavior of GBM tumors. Genipin can downregulate the expression of GPX4 and upregulate the expression of ACSL4 by inhibiting UCP2, leading to ferroptosis and alleviating the malignant behavior of tumors. In summary, UCP2 is a potential therapeutic target for GBM. Genipin, which targets UCP2, effectively inhibits GBM development by inducing ferroptosis in vivo and in vitro. These findings indicate that genipin treatment based on UCP2 targeting has potential therapeutic applications with a clinical perspective for the treatment of GBM patients.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025221
Hypertension is commonly accompanied by endothelial dysfunction, characterized by an imbalance between vasodilatation and constriction, increased levels of the proinflammatory factors interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1), and decreased nitric oxide (NO) bioavailability. Using an angiotensin II (Ang II)-induced endothelial dysfunction model, we show that treatment with the hydrogen sulfide (H₂S) donor GYY4137 significantly reverses Ang II-induced damage. GYY4137 restores sirtuin 6 (SIRT6) expression, suppresses inflammation, and improves vasodilatory function. Furthermore, endothelial-specific cystathionine-γ-lyase (CSE)-deficient mice exhibit inflammation and endothelial dysfunction in blood vessels, which is reversed by H₂S supplementation. Critically, SIRT6 inhibitors block the protective effects of H₂S in the endothelium. This study demonstrates that H₂S protects vascular endothelial function by activating the SIRT6 anti-inflammatory pathway.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024122
The main protease (Mpro) of coronaviruses plays a key role in viral replication, thus serving as a hot target for drug design. PF-00835231 is a promising inhibitor of SARS-CoV-2 Mpro. Here, we report the inhibitory potency of PF-00835231 against SARS-CoV-2 Mpro and seven Mpro mutants (G15S, M49I, Y54C, K90R, P132H, S46F, and V186F) from SARS-CoV-2 variants. The results confirm that PF-00835231 has broad-spectrum inhibition against various coronaviral Mpros. In addition, the crystal structures of SARS-CoV-2 Mpro, SARS-CoV Mpro, MERS-CoV Mpro, and seven SARS-CoV-2 Mpro mutants (G15S, M49I, Y54C, K90R, P132H, S46F, and V186F) in complex with PF-00835231 are solved. A detailed analysis of these structures reveals key determinants essential for inhibition and elucidates the binding modes of different coronaviral Mpros. Given the importance of the main protease for the treatment of coronaviral infection, structural insights into Mpro inhibition by PF-00835231 can accelerate the design of novel antivirals with broad-spectrum efficacy against different human coronaviruses.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024110
Immune checkpoint inhibitors (ICIs) targeting programmed cell death 1/programmed cell death ligand-1 (PD-1/PD-L1) have significantly prolonged the survival of advanced/metastatic patients with lung cancer. However, only a small proportion of patients can benefit from ICIs, and clinical management of the treatment process remains challenging. Glycosylation has added a new dimension to advance our understanding of tumor immunity and immunotherapy. To systematically characterize anti-PD-1/PD-L1 immunotherapy-related changes in serum glycoproteins, a series of serum samples from 12 patients with metastatic lung squamous cell carcinoma (SCC) and lung adenocarcinoma (ADC), collected before and during ICIs treatment, are firstly analyzed with mass-spectrometry-based label-free quantification method. Second, a stratification analysis is performed among anti-PD-1/PD-L1 responders and non-responders, with serum levels of glycopeptides correlated with treatment response. In addition, in an independent validation cohort, a large-scale site-specific profiling strategy based on chemical labeling is employed to confirm the unusual characteristics of IgG N-glycosylation associated with anti-PD-1/PD-L1 treatment. Unbiased label-free quantitative glycoproteomics reveals serum levels’ alterations related to anti-PD-1/PD-L1 treatment in 27 out of 337 quantified glycopeptides. The intact glycopeptide EEQFN177STYR (H3N4) corresponding to IgG4 is significantly increased during anti-PD-1/PD-L1 treatment (FC=2.65, P=0.0083) and has the highest increase in anti-PD-1/PD-L1 responders (FC=5.84, P=0.0190). Quantitative glycoproteomics based on protein purification and chemical labeling confirms this observation. Furthermore, obvious associations between the two intact glycopeptides (EEQFN177STYR (H3N4) of IgG4, EEQYN227STFR (H3N4F1) of IgG3) and response to treatment are observed, which may play a guiding role in cancer immunotherapy. Our findings could benefit future clinical disease management.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2024139
Esophageal cancer (EC) is one of the most recalcitrant cancers, with a 5-year survival rate of < 30%. The hydroxyacyl-CoA dehydrogenase alpha subunit (HADHA) plays an essential role in long-chain fatty acid metabolism, and dysregulation of HADHA has been demonstrated to be involved in a series of metabolic diseases and cancers. However, its role in cancers remains controversial. HADHA has seldom been investigated in EC, and little is known about how HADHA regulates the malignant progression of EC. In this study, we find that HADHA is significantly upregulated in EC tissues and is correlated with poor survival. HADHA knockdown markedly inhibits EC cell proliferation both in vitro and in vivo. The loss of HADHA also induces EC cell apoptosis, causes cell cycle arrest and inhibits cell migration. Additionally, RNA profiling reveals that mTOR signaling is significantly suppressed after HADHA knockdown. Mechanistically, HADHA interacts with SP1 and induces MDM2 expression. In conclusion, both mTOR signaling and the SP1-MDM2 axis participate in the HADHA-induced malignant behavior of EC cells.
Stem Cell Research & Therapy•2026•DOI: 10.1186/s13287-026-05026-0
Osteonecrosis of the femoral head (ONFH) is a progressive orthopedic disorder culminating in femoral head collapse and joint failure. Dysfunction of bone marrow mesenchymal stem cells (BMSCs), including impaired osteogenesis, enhanced adipogenesis, and mitochondrial dysfunction, is a central driver of ONFH pathogenesis. Paired BMSCs were isolated from necrotic femoral head regions (fhBMSCs) and the iliac crest (iBMSCs) of ONFH patients. Functional assays, RNA sequencing, and molecular analyses evaluated the effects of the hypoxia mimetic dimethyloxalylglycine (DMOG) on osteogenic–adipogenic balance, mitochondrial function, and senescence. Loss-of-function experiments targeting hypoxia-inducible factor-1α (HIF-1α) and Homer3 elucidated mechanistic pathways. Compared with iBMSCs, fhBMSCs exhibited impaired osteogenesis, enhanced adipogenesis, mitochondrial dysfunction, and increased senescence. DMOG pretreatment restored osteogenic differentiation, suppressed adipogenesis, improved mitochondrial dynamics, reduced oxidative stress, and enhanced bioenergetic metabolism. These protective effects were dependent on HIF-1α stabilization. Transcriptomic profiling identified Homer3 as a downstream negative regulator of HIF-1α. Homer3 was aberrantly upregulated in fhBMSCs but suppressed by DMOG, and its knockdown mimicked the effects of DMOG by promoting osteogenesis, inhibiting adipogenesis, enhancing mitophagy, and restoring mitochondrial function. Conversely, silencing HIF-1α abolished DMOG-mediated benefits and reinstated Homer3 expression. These findings suggest that pharmacological targeting of the HIF-1α/Homer3 axis may represent a novel joint-preserving strategy for ONFH.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025148
Mesothelial cells play an important role in colorectal cancer peritoneal metastasis (CRC-PM), where they support tumor growth and invasion. In this study, we investigate the molecular mechanisms by which mesothelial cells contribute to CRC metastasis. Using single-cell RNA sequencing (scRNA-seq) on tissue samples from 12 CRC patients with peritoneal metastasis, we identify PDK4 as a key gene in mesothelial cells during metastasis. The expression of PDK4 is significantly greater in mesothelial cells undergoing mesothelial-to-mesenchymal transition (MMT) compared to normal peritoneal cells, suggesting its involvement in mesothelial cell reprogramming during peritoneal metastasis. In vitro experiments show that coculturing mesothelial cells with CRC cells leads to increased PDK4 expression, which in turn enhances mesothelial cell migration and invasion. Knockdown of PDK4 reduces mesothelial cell invasion, while overexpression of PDK4 increases invasive ability, highlighting its critical role in mesothelial cell invasion. Additionally, PDK4 promotes metabolic changes, specifically increasing fatty acid oxidation (FAO), which is necessary for mesothelial cell invasion. Blocking FAO reduces the invasive ability of PDK4-overexpressing mesothelial cells, while restoring FAO in PDK4-knockdown cells rescues their invasion potential. Further analysis shows that PDK4 enhances the acetylation of β-catenin, a protein involved in cell movement, and that this modification is crucial for mesothelial cell invasion. Our results suggest that PDK4 regulates mesothelial cell invasion through β-catenin acetylation following metabolic reprogramming, offering a potential target for therapies aimed at inhibiting CRC-PM.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21376
OBJECTIVE: This study aimed to systematically compare the efficacy and safety of various neuromodulation techniques for upper limb motor function recovery after stroke, and to rank the relative advantages of different interventions through a network meta-analysis, thereby providing evidence-based guidance for clinical rehabilitation. METHODS: A comprehensive literature search was conducted in CNKI, WanFang, VIP, CBM, PubMed, EMbase, Web of Science, and Cochrane Library from inception to August 2025. Randomized controlled trials investigating different neuromodulation techniques for post-stroke upper limb motor impairment were included. Control group received sham stimulation or conventional rehabilitation, while trial group received additional neuromodulation therapies. The methodological quality of included studies was assessed using the Cochrane Risk of Bias Tool. Network meta-analyses were performed using Stata 16.0 and RevMan 5.4 software. RESULTS: A total of 51 randomized controlled trials were included, covering 12 neuromodulation stimulation modalities. Network meta-analysis results showed that compared with conventional treatment, high-frequency repetitive transcranial magnetic stimulation (MD=11.50, 95%CI: 6.83-16.16, P < 0.05) was most effective in improving basic upper limb motor function recovery; continuous theta burst stimulation (MD=12.10, 95%CI: 44.99-19.21, P < 0.05; MD=9.60, 95%CI: 1.32-17.88, P < 0.05) was most effective in improving the practicality and dexterity of upper limb function; and cathodal transcranial direct current stimulation (MD=15.40, 95%CI: 0.03-30.77, P < 0.05; MD=-0.83, 95%CI: -1.64 to -0.03, P < 0.05) was most effective in improving daily living activity limitations or with obvious spasticity. CONCLUSION: When the goal is to promote basic upper limb motor function recovery, high-frequency repetitive transcranial magnetic stimulation is most effective; for improving the practicality and dexterity of upper limb function, continuous theta burst stimulation is most effective; and for patients with impaired daily living ability accompanied by obvious spasticity, cathodal transcranial direct current stimulation is most effective.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21504
BACKGROUND: With the deepening of China's aging population, low skeletal muscle mass has become a serious public health problem. Diet is closely linked to muscle mass; however, existing research has mostly focused on the effects of a single nutrient, and there is still a lack of systematic exploration of the relationship between China's overall dietary pattern and skeletal muscle quality. OBJECTIVE: To analyze the correlation between Chinese Healthy Eating Index and skeletal muscle mass in older adults, providing scientific basis for dietary optimization and prevention of low skeletal muscle mass. METHODS: Based on the 2018 China Longitudinal Healthy Longevity Survey (CLHLS), 8,114 participants were included. Dietary quality was assessed using the Chinese Healthy Eating Index, and skeletal muscle mass was evaluated using the skeletal muscle mass index. Low skeletal muscle mass was diagnosed according to the 2019 Asian Working Group for Sarcopenia criteria. Multivariate logistic regression was used to explore the association between Chinese Healthy Eating Index and low skeletal muscle mass. RESULTS AND CONCLUSION: (1) Univariate analysis showed that the highest quartile (Q4) of overall Chinese Healthy Eating Index (OR=0.52, 95%CI: 0.46-0.59), animal-based Chinese Healthy Eating Index (OR=0.85, 95%CI: 0.75-0.97), and plant-based Chinese Healthy Eating Index (OR=0.43, 95%CI: 0.38-0.49) were significantly associated with low skeletal muscle mass (P < 0.001). (2) Multivariate logistic regression showed that compared with the lowest quartile (Q1), the highest quartile (Q4) of overall, animal-based, and plant-based Chinese Healthy Eating Index were associated with 30% (OR=0.70, 95%CI: 0.60-0.83, P < 0.05), 20% (OR=0.80, 95%CI: 0.68-0.94, P < 0.05), and 20% (OR=0.80, 95%CI: 0.69-0.94, P < 0.05) lower risk of low skeletal muscle mass, respectively. Trend tests further indicated a significant association between higher dietary quality and lower risk of low skeletal muscle mass (P_trend < 0.001). (3) Subgroup analysis showed that in female participants, compared with Q1, the highest quartile (Q4) of overall, animal-based, and plant-based Chinese Healthy Eating Index were associated with 43% (OR=0.57, 95%CI: 0.45-0.72, P < 0.05), 29% (OR=0.71, 95%CI: 0.56-0.88, P < 0.001), and 33% (OR=0.67, 95%CI: 0.54-0.83, P < 0.001) lower risk of low skeletal muscle mass, respectively. No significant association was found in males. The results indicate that higher dietary quality is significantly associated with lower risk of low skeletal muscle mass, and adopting a healthy diet is an effective intervention to prevent skeletal muscle loss.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026066
Fibroblast growth factor 10 (FGF10) plays a critical role in ocular surface homeostasis, yet its function in early meibomian gland (MG) development remains largely unknown. Here, we generated an Fgf10 mutant mouse model with deletion of exon 2, leading to loss of function. Adult Fgf10+/− mice exhibited lacrimal gland agenesis, smaller Harderian glands, increased corneal fluorescein staining, and reduced tear volume. Histological analysis revealed multilayered hyperplastic epithelium in Harderian glands and MG atrophy. Time-series Oil Red O staining showed shorter, thinner, and disordered MGs in Fgf10+/− mice at P14 and P21, with unrecoverable defects at P135. RNA sequencing of MGs at P14 and P21 revealed significant dysregulation of macrophage-related genes and immune-related pathways, including antigen processing and presentation and macrophage chemotaxis. Using Cx3cr1GFP/+ reporter mice, we observed a significant reduction in CX3CR1-positive cells in the inter-acinar stroma of Fgf10+/− MGs. Pharmacological ablation of CSF1R-expressing cells with PLX3397 in wild-type mice recapitulated the MG developmental defects, confirming that FGF10 acts through immune cells to regulate MG development. Collectively, our findings establish that FGF10 haploinsufficiency leads to severe glandular malformations, impaired tear production, and compromised corneal integrity, highlighting the essential role of FGF10 in postnatal MG development and immune cell regulation.
Chinese Journal of Pathophysiology•2026•DOI: 10.3969/j.issn.1000-4718.2026.05.014
AIM: Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and immune dysregulation, yet the spatial epigenetic and neuroimmune features within the skin remain poorly understood. This study aims to construct a spatial atlas of the neuroimmune and epigenetic microenvironment in psoriasis. METHODS: Formalin-fixed, paraffin-embedded skin tissue samples from five psoriasis patients and four healthy controls were stained with a 33-metal antibody panel targeting immune and epigenetic markers. Imaging data were processed to analyze immune cell composition, spatial relationships, and epigenetic marker distribution in psoriatic lesions. RESULTS: Analysis of over 163,000 cells from five psoriasis patients and four healthy controls revealed that psoriatic lesions have a more complex cellular composition than normal skin, including diverse immune subsets, endothelial cells, keratinocytes, and nerve fibers. Neighborhood analysis showed enrichment of multiple immune cells, such as CD14+ monocytes, CD4+/CD8+ T-lymphocytes (T cells), CD68+ macrophages, CD69+ tissue-resident memory T cells and CD20+ B-lymphocytes (B cells), and nerve fibers around keratinocytes. Notably, positive interactions were observed between cutaneous nerve fibers and specific immune cells (CD8+ T cells and CD68+ macrophages) as well as blood vessels. Additionally, histone H3 lysine 27 trimethylation (H3K27me3) modification was mapped across cell types and found in immune cells adjacent to keratinocytes. CONCLUSION: Imaging mass cytometry delineated the psoriatic microenvironment's multicellular structure integrating epigenetic and neuroimmune components, offering new insights into psoriasis pathogenesis.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025221
Hypertension is commonly accompanied by endothelial dysfunction, characterized by an imbalance between vasodilatation and constriction, increased levels of the proinflammatory factors interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1), and decreased nitric oxide (NO) bioavailability. Using an angiotensin II (Ang II)-induced endothelial dysfunction model, we show that treatment with the hydrogen sulfide (H₂S) donor GYY4137 significantly reverses Ang II-induced damage. GYY4137 restores sirtuin 6 (SIRT6) expression, suppresses inflammation, and improves vasodilatory function. Furthermore, endothelial-specific cystathionine-γ-lyase (CSE)-deficient mice exhibit inflammation and endothelial dysfunction in blood vessels, which is reversed by H₂S supplementation. Critically, SIRT6 inhibitors block the protective effects of H₂S in the endothelium. This study demonstrates that H₂S protects vascular endothelial function by activating the SIRT6 anti-inflammatory pathway.