Objective: To evaluate the clinical efficacy and safety of injectable platelet-rich fibrin (i-PRF) in the treatment of mild to moderate female pattern hair loss (FPHL), and to analyze the related clinical factors affecting the therapeutic efficacy of i-PRF. Methods: This was a secondary analysis of a prospective, randomized controlled trial. A total of 29 FPHL patients with Sinclair grade Ⅱ-Ⅲ, who attended the outpatient clinics of Beijing Friendship Hospital, Capital Medical University and Peking University Third Hospital from March 2024 to April 2025, were enrolled. All patients received i-PRF treatment once every 4 weeks for a total of 4 sessions, with follow-up up to 24 weeks. Standardized clinical photographs were taken at baseline, week 12 and week 24. Trichoscopic examination was performed to measure the non-vellus target area hair count (TAHC) and hair diameter (HD) in the target area, and all adverse events were recorded. The Mann-Whitney U test was used to compare the intergroup differences in efficacy for categorical influencing factors; Spearman rank correlation analysis was employed to assess the correlation between continuous influencing factors and efficacy; and multiple linear regression (enter method) was performed to identify independent influencing factors of efficacy. Results: A total of 27 patients completed the trial. At week 12, TAHC significantly increased from 112 (105, 120) hairs/cm at baseline to 128 (110, 150) hairs/cm , with a median increase of 12 (5, 28) hairs/cm and a median growth rate of 10.5 (4.2, 24.5)% (P=0.045); hair diameter significantly increased from 42.5 (39.8, 45.2) μm to 52.0 (47.0, 58.0) μm, with a median increase of 7.5 (3.0, 12.5) μm and a median growth rate of 18.0 (7.5, 29.0)% (P<0.001). At week 24, TAHC further significantly increased to 141 (125, 158) hairs/cm (P<0.001), with a median growth rate of 24.8 (18.5, 32.0)%; hair diameter continued to improve to 55.0 (50.0, 61.0) μm (P=0.008), with a median growth rate of 21.5 (16.0, 27.0)%. The overall incidence of adverse events was 10.34% (3/29), mainly presenting as mild scalp pruritus and transient headache, without severe adverse effects. Multiple linear regression analysis revealed that baseline TAHC was an independent influencing factor for i-PRF efficacy (P<0.05), while age, BMI, disease duration, Sinclair grade, family history of AGA, and baseline HD showed no significant independent effect on efficacy in this model (P>0.05). Conclusion: This preliminary study indicates that i-PRF can improve hair density and hair shaft diameter in patients with FPHL with a favorable safety profile. Patients with FPHL and lower baseline TAHC may achieve greater clinical improvement.

OBJECTIVE To investigate the clinical efficacy and safety of Zhengxintai granules as in the treatment of microvascular angina （MVA） following percutaneous coronary intervention （PCI） in patients with acute ST-segment elevation myocardial infarction （STEMI） and qi deficiency and blood stasis syndrome. METHODS Patients with STEMI and qi deficiency and blood stasis syndrome who underwent PCI and developed MVA and were admitted to the Jinan Fourth People’s Hospital （Jinan Cardiovascular Hospital） from March 2022 to March 2025 were selected， they were randomly divided into the control group and the observation group according to a random number table， with 76 cases in each group. Patients in the control group received conventional Western medicine treatment combined with a placebo， while patients in the observation group received Zhengxintai granules （5 mg per dose， three times daily， for 8 weeks） in addition to conventional Western medicine treatment. The clinical efficacy [including the total effective rate of traditional Chinese medicine （TCM） syndrome improvement and the total effective rates of Western clinical efficacy] was compared between the two groups. The following indicators were detected before and after treatment： TCM syndrome scores， angina pectoris episodes [daily attack frequency， duration per attack， Visual Analogue Scale （VAS） score]， cardiac function indicators [lactate dehydrogenase （LDH）， N-terminal pro-B-type natriuretic peptide （NT-proBNP）， left ventricular end-diastolic dimension （LVEDD）， left ventricular end-systolic dimension （LVESD）， left ventricular ejection fraction （LVEF）， cardiac output （CO）， fractional shortening （FS）]， coagulation function indicators [thrombin time （TT）， prothrombin time （PT）， fibrinogen （FIB）]， fibrinolytic marker （D-dimer）， vascular endothelial function indicators [vascular endothelial growth factor （VEGF）， nitric oxide （NO）， endothelin-1 （ET-1）] and myocardial microcirculation hemodynamic indicators [end-diastolic velocity （EDV）， peak systolic velocity （PSV）， resistance index （RI）， pulsatility index （PI）]. The quality of life [Seattle Angina Questionnaire （SAQ） score] and the incidence of adverse reactions were also compared between the two groups. RESULTS There was no patient dropout during the entire course of the study. The total effective rates of improvement in TCM syndromes and the total effective rates of Western clinical efficacy in the observation group were significantly higher than those in the control group （93.42% vs. 82.89%， 94.74% vs. 84.21%， P＜0.05）. Before the treatment， the comparison of each examination indicator between the two groups showed no statistically significant differences （P＞0.05）. Compared with before treatment， the TCM syndrome scores， the number of daily angina pectoris attacks and the duration of each attack， the VAS scores， LDH， NT-proBNP， FIB， D-dimer， ET-1 levels， LVEDD， LVESD， RI and PI after treatment in both groups were significantly reduced， shortened or decreased （P＜0.05）； VEGF and NO levels， LVEF， CO， FS， TT， PT， EDV， PSV， and the standard scores of five dimensions including angina pectoris stability， as well as the total scores of SAQ， all significantly increased or prolonged （P＜0.05）. Furthermore， the improvements in the aforementioned indicators （except for LVEF） in the observation group were significantly greater than those in the control group （P＜0.05）. There was no statistically significant difference in the total incidence of adverse reactions between the two groups （P＞0.05）. CONCLUSIONS Zhengxintai granules， when used as an adjunct to conventional Western medicine， can significantly alleviate the related symptoms of MVA in STEMI patients with qi deficiency and blood stasis syndrome after PCI， repair damaged cardiac function， restore the balance of the coagulation-fibrinolysis system， improve vascular endothelial function and myocardial microcirculation perfusion， and significantly enhance the quality of life of patients

Lung cancer is the malignant tumor with the highest incidence and mortality rates globally. Current treatment methods for lung cancer primarily include surgery， chemotherapy， targeted therapy， and immunotherapy. However， the main limitations of these treatments are their side effects， the drug resistance， and the economic burden they impose. As a critical cancer pathway， the Janus kinase （JAK）/signal transducer and activator of transcription （STAT） signaling pathway regulates tumor occurrence and development through multiple mechanisms by influencing various downstream targets. Consequently， the JAK/STAT signaling pathway offers a promising avenue for lung cancer treatment research. Numerous studies have demonstrated that the JAK/STAT signaling pathway plays a key role in the proliferation and growth of lung cancer cells， angiogenesis， epithelial-mesenchymal transition （EMT）， metabolic alterations， remodeling of the immune microenvironment， and the development of treatment resistance. Traditional Chinese medicine （TCM） has garnered increasing attention due to its minimal side effects， low economic burden， and its potential to enhance efficacy and reduce toxicity when used in conjunction with Western medicine. In addition to traditional Chinese medicine compounds， a growing number of Chinese medicine monomers have come into the spotlight because of their more targeted effects. Numerous studies investigating the regulation of the JAK/STAT signaling pathway by TCM in the treatment of lung cancer have demonstrated that TCM can inhibit the proliferation and invasion of lung cancer cells， tumor angiogenesis， and EMT， improve the inflammatory and immunosuppressive microenvironments， and enhance treatment sensitivity by intervening in the JAK/STAT signaling pathway， thereby impeding the progression of lung cancer. In recent years， the research on the regulation of this pathway by TCM in the treatment of lung cancer has been updated rapidly. However， the summary of these studies has not been updated in time. This review summarizes and reflects on the recent research findings regarding the regulation of the JAK/STAT signaling pathway by TCM to intervene in lung cancer from three aspects， introducing the JAK/STAT pathway， elaborating the mechanism of this pathway in lung cancer， and exploring the intervention of TCM in the treatment of lung cancer through this pathway， to provide more reference for the treatment of lung cancer in the future.

Objective To screen antidepressant-active compounds from Polygonati Rhizoma and explore their effects and possible mechanisms against depression induced by simulated weightlessness.Methods A systems pharmacology approach was used to screen potential antidepressant-active compounds and their targets from Polygonati Rhizoma.The hindlimb unloading(HLU)rat model was employed for the study.Twenty-four healthy male Sprague-Dawley rats were randomly divided into three groups:control group(administered 0.5%carboxymethylcellulose by gavage),HLU group(hindlimb unloading),and HLU+treatment group(hindlimb unloading+active compound gavage),with 8 rats in each group.After 28 days of hindlimb unloading,depressive-like behaviors in rats were evaluated using the forced swimming test and tail suspension test.Hippocampal morphology was examined with H&E staining,and GO and KEGG enrichment analyses were conducted on the targets of active compounds.Results A total of 38 active compounds were screened from Polygonati Rhizoma,among which apigenin had an oral bioavailability of 23.06%and a drug-likeness score of 0.21.Compound-target network analysis indicated that apigenin had the highest degree and betweenness centrality values,suggesting it might be the key active component with antidepressant potential in Polygonati Rhizoma.In the forced swimming and tail suspension tests,rats in the HLU group showed a significant increase in immobility time compared to the control group,indicating successful establishment of the depression model.However,compared to the HLU group,rats in the HLU plus apigenin group exhibited significantly reduced immobility time.The H&E staining results of hippocampal tissue showed a significant reduction in the number of hippocampal neurons,along with numerous shrunken neurons and small vacuoles in nerve fibers in the HLU group.In contrast,the treatment group exhibited an increased number of hippocampal neurons,with improved cellular morphology.Target enrichment analysis indicated that apigenin targets were mainly involved in the regulation of apoptosis and cancer-related signaling pathways.Conclusion Apigenin significantly improved depressive-like behaviors in rats subjected to hindlimb unloading,and it has a protective effect on hippocampal tissue.It may provide a new natural active compound for the treatment of depression caused by spaceflight-induced weightlessness.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent cause of chronic liver disease worldwide, and its intricate pathogenesis presents challenges in the development of new drugs. As a common way of post-translational modification, acetylation regulates protein stability, enzyme activity, and subcellular localization, occurring extensively in MASLD-associated processes such as lipid metabolism, inflammatory response, and oxidative stress. In this paper, we comprehensively review the mechanism of acetylation in MASLD, analyze the expression levels of acetylases in liver tissues of MASLD patients from the gene expression omnibus (GEO), discuss the changes in relevant enzyme expression and mechanisms in animal models, and further explore the feasibility of targeting acetylation for MASLD treatment, in the hope of offering a new perspective for advancing drug discovery in the field of MASLD.

Diabetic kidney disease(DKD)with increasing global prevalence lacks effective therapeutic targets to halt or reverse its progression.Therapeutic targets supported by causal genetic evidence are more likely to succeed in randomized clinical trials.In this study,we integrated large-scale plasma proteomics,genetic-driven causal inference,and experimental validation to identify prioritized targets for DKD using the UK Biobank(UKB)and FinnGen cohorts.Among 2844 diabetic patients(528 with DKD),we identified 37 targets significantly associated with incident DKD,supported by both observational and causal evi-dence.Of these,22％(8/37)of the potential targets are currently under investigation for DKD or other diseases.Our prospective study confirmed that higher levels of three prioritized targets-insulin-like growth factor binding protein 4(IGFBP4),family with sequence similarity 3 member C(FAM3C),and prostaglandin D2 synthase(PTGDS)—were associated with a 4.35,3.51,and 3.57-fold increased likeli-hood of developing DKD,respectively.In addition,population-level protein-altering variants(PAVs)analysis and in vitro experiments cross-validated FAM3C and IGFBP4 as potential new target candidates for DKD,through the classic NLR family pyrin domain containing 3(NLRP3)-caspase-1-gasdermin D(GSDMD)apoptotic axis.Our results demonstrate that integrating omics data mining with causal inference may be a promising strategy for prioritizing therapeutic targets.

Several types of arthritis share the common feature that the generation of inflammatory mediators leads to joint cartilage degradation. However, the shared mechanism is largely unknown. H2BK120ub1 was reportedly involved in various inflammatory diseases but its role in the shared mechanism in inflammatory joint conditions remains elusive. The present study demonstrated that levels of cartilage degradation, H2BK120ub1, and its regulator WW domain-containing adapter protein with coiled-coil (WAC) were increased in cartilage in human rheumatoid arthritis (RA) and osteoarthritis (OA) patients as well as in experimental RA and OA mice. By regulating H2BK120ub1 and H3K27me3, WAC regulated the secretion of inflammatory and cartilage-degrading factors. WAC influenced the level of H3K27me3 by regulating nuclear entry of the H3K27 demethylase KDM6B, and acted as a key factor of the crosstalk between H2BK120ub1 and H3K27me3. The cartilage-specific knockout of WAC demonstrated the ability to alleviate cartilage degradation in collagen-induced arthritis (CIA) and collagenase-induced osteoarthritis (CIOA) mice. Through molecular docking and dynamic simulation, doxercalciferol was found to inhibit WAC and the development of cartilage degradation in the CIA and CIOA models. Our study demonstrated that WAC is a key factor of cartilage degradation in arthritis, and targeting WAC by doxercalciferol could be a viable therapeutic strategy for treating cartilage destruction in several types of arthritis.

Oligodendrocyte lineage cells, including oligodendrocyte precursor cells (OPCs) and oligodendrocytes (OLs), are essential in establishing and maintaining brain circuits. Autophagy is a conserved process that keeps the quality of organelles and proteostasis. The role of autophagy in oligodendrocyte lineage cells remains unclear. The present study shows that autophagy is required to maintain the number of OPCs/OLs and myelin integrity during brain aging. Inactivation of autophagy in oligodendrocyte lineage cells increases the number of OPCs/OLs in the developing brain while exaggerating the loss of OPCs/OLs with brain aging. Inactivation of autophagy in oligodendrocyte lineage cells impairs the turnover of myelin basic protein (MBP). It causes MBP to accumulate in the cytoplasm as multimeric aggregates and fails to be incorporated into integral myelin, which is associated with attenuated endocytic recycling. Inactivation of autophagy in oligodendrocyte lineage cells impairs myelin integrity and causes demyelination. Thus, this study shows autophagy is required to maintain myelin quality during aging by controlling the turnover of myelin components.
Animals ; Autophagy/physiology* ; Oligodendroglia/metabolism* ; Myelin Sheath/physiology* ; Aging/pathology* ; Myelin Basic Protein/metabolism* ; Cell Lineage/physiology* ; Mice ; Oligodendrocyte Precursor Cells ; Mice, Inbred C57BL ; Brain/cytology* ; Cells, Cultured ; Cell Count

Diabetic kidney disease (DKD) with increasing global prevalence lacks effective therapeutic targets to halt or reverse its progression. Therapeutic targets supported by causal genetic evidence are more likely to succeed in randomized clinical trials. In this study, we integrated large-scale plasma proteomics, genetic-driven causal inference, and experimental validation to identify prioritized targets for DKD using the UK Biobank (UKB) and FinnGen cohorts. Among 2844 diabetic patients (528 with DKD), we identified 37 targets significantly associated with incident DKD, supported by both observational and causal evidence. Of these, 22% (8/37) of the potential targets are currently under investigation for DKD or other diseases. Our prospective study confirmed that higher levels of three prioritized targets-insulin-like growth factor binding protein 4 (IGFBP4), family with sequence similarity 3 member C (FAM3C), and prostaglandin D2 synthase (PTGDS)-were associated with a 4.35, 3.51, and 3.57-fold increased likelihood of developing DKD, respectively. In addition, population-level protein-altering variants (PAVs) analysis and in vitro experiments cross-validated FAM3C and IGFBP4 as potential new target candidates for DKD, through the classic NLR family pyrin domain containing 3 (NLRP3)-caspase-1-gasdermin D (GSDMD) apoptotic axis. Our results demonstrate that integrating omics data mining with causal inference may be a promising strategy for prioritizing therapeutic targets.