Yunnan Provincial Hospital of Traditional Chinese Medicine

Cellular senescence is a fundamental biological program that enforces a stable cell-cycle arrest in response to diverse stresses, acting as a crucial barrier against malignant transformation. In the context of prostate cancer, however, this protective mechanism paradoxically exhibits tumor-promoting potential under certain microenvironmental and therapeutic conditions. This review examines the various aspects of senescence in prostate cancer development, ranging from DNA damage- and oncogene-induced senescence (p53/p21, PTEN/p16, and RAS/MYC) to treatment-induced senescence following androgen deprivation, radiotherapy, and chemotherapy. While senescence temporarily halts tumor formation via cell-intrinsic checkpoints and immune surveillance, overly persistent senescent cells trigger the development of a senescence-associated secretory phenotype (SASP) in which they secrete proinflammatory cytokines, chemokines, and proteases that modify the tumor microenvironment in ways that encourage inflammation, assist in the hyper-epithelial plasticity, and therapeutic resistance of the tumor. This review highlights new insights into the epigenetic control and metabolic rewiring that determine the shift between tumor-suppressing senescence and tumor-promoting senescence. This review consolidates the paradox of 'double-edged sword' senescence, delineating that its impact is contextually dependent on the cell, immune environment, and the duration of senescence. Finally, we discuss the predicted therapeutic approaches based on precision oncology to target and alter senescence using senolytics to eradicate aberrant senescent cells and senomorphics to target and adjust SASP. Addressing and regulating the plasticity of senescence is a significant and critical opportunity for improving the prognosis of prostate cancer, as well as guiding next-generation senescence-informed therapeutic approaches.

Myopia has emerged as a major threat to the visual health of adolescents worldwide. Early intervention can effectively slow down the progression of myopia in adolescents. Tuina (also known as Tui Na), a significant therapeutic method in traditional Chinese medicine, has shown promising clinical efficacy in delaying the progression of myopia; however, it lacks robust, large-scale, and standardized randomized controlled trials. This study aims to explore the efficacy and safety of tuina therapy in managing myopia in adolescents, thereby providing solid evidence for the application of tuina in the clinical treatment of myopia. This study is a multicenter randomized controlled clinical trial. A total of 62 children with myopia will be recruited from 4 hospitals and randomly assigned in a 1:1 ratio to a tuina experimental group and a drug-positive control group (tropicamide eye drops). Treatments in each group will be administered 3 times per week for a total of 8 weeks. The tuina experimental group will receive 20 minutes of tuina therapy per session, while the drug-positive control group will receive tropicamide eye drops administered every other day, with 2 drops per session. The primary outcome measures include uncorrected visual acuity and axial length, while secondary outcome measures include refractive power and accommodative amplitude. Data will be collected at baseline (week 0), on the day of completion of weeks 4 and 8 of treatment, and at the end of the 10-week follow-up period. Adverse events will be monitored and recorded throughout the study. Statisticians will be blinded. Data will be analyzed using SPSS version 28.0. This study has been funded, and recruitment began in June 2025. As of December 2025, 29 participants have been enrolled, with 16 allocated to the tuina group and 13 to the drug-positive control group. Recruitment is expected to continue until October 2026. Final manuscript submission is anticipated by December 2026. This study aims to evaluate the efficacy and safety of tuina therapy in the treatment of adolescents with myopia. We hypothesize that the therapeutic effect of tuina therapy is noninferior to that of tropicamide eye drops, with the additional advantages of fewer side effects and stable long-term efficacy, thereby providing reliable evidence and support for the application of tuina therapy in the management of myopia in adolescents.

Polycystic ovary syndrome (PCOS) is a common gynaecological endocrine disorder that affects women of reproductive age and is often accompanied by clinical symptoms such as acne, obesity, menstrual disorders, and ovulation disorders. Although the molecular mechanisms underlying the pathophysiology of PCOS are still unknown despite the condition’s extremely complex underlying mechanism, recent studies suggest that glycolysis may be involved in PCOS pathogenesis, including hyperandrogenism, inflammation, ovulatory dysfunction, and diminished endometrial receptivity and infertility. Therefore, there is an urgent need to explore the pathogenesis and treatment of glycolysis in patients with PCOS. The present review discusses the mechanism of glycolysis, the association between glycolysis and diverse features of PCOS, the molecular mechanism underlying the involvement of glycolysis in the pathogenesis of PCOS, and some common treatment strategies involving glycolysis in patients with PCOS. More prospective studies using advanced detection technologies such as Seahorse are needed to elucidate the specific molecular mechanisms through which glycolysis is involved in the pathogenesis of PCOS.

BackgroundNeutrophil extracellular traps (NETs) contribute significantly to osteoarthritis (OA) pathogenesis; however, the precise molecular interactions remain unclear. This study aimed to identify key NET-associated genes and their correlated metabolites and microbiota in OA through an integrated multi-omics approach.MethodsInitially, transcriptomic datasets were screened to identify NET-related genes implicated in OA. A rat OA model was established, and the expression of key genes was validated using RT-qPCR, histological analysis, and immunohistochemistry. TIMP1 was selected for further exploration via in vivo gene silencing. Subsequently, transcriptomics, metabolomics, and 16S rRNA sequencing were performed on serum, cartilage, and fecal samples from experimental animals. Differentially expressed genes (DEGs), microbiota, and metabolites associated with TIMP1 were identified through integrated bioinformatics analyses. Correlation analyses across omics data layers were conducted to pinpoint biomarkers, key metabolites, and microbial taxa.ResultsITGB1, ITGB2, MMP9, and TIMP1 emerged as key NET-associated genes, with TIMP1 being selected as the primary target. TIMP1 silencing significantly alleviated inflammatory responses and cartilage degradation in OA rats. Multi-omics analyses identified 6 biomarkers, 9 key metabolites (e.g., FAHFAs, 12-HETE, MTA, xanthosine), and 1 key microbial genus (Muribaculaceae) strongly correlated with TIMP1 expression. These molecular entities were enriched in pathways related to lipid metabolism, nucleotide turnover, immune regulation, and gut-joint crosstalk.ConclusionTIMP1 acts as a pivotal regulator in OA, influencing inflammation, cartilage remodeling, metabolic pathways, and gut microbiota composition. This study provides novel mechanistic insights and potential therapeutic targets for OA.

Chronic obstructive pulmonary disease (COPD), a leading global cause of mortality and morbidity, imposes substantial socioeconomic burdens due to its progressive nature and limited therapeutic efficacy. Current strategies face dual challenges: suboptimal pulmonary bioavailability of pharmacologic agents and systemic toxicity from non-targeted drug distribution. To address these limitations, this review establishes a mechanistic framework through the first systematic identification of COPD-specific nano-intervention targets, organized around four core pathophysiological axes: (1) dysregulated inflammatory cascades, (2) redox imbalance mechanisms, (3) protease-antiprotease homeostasis disruption, and (4) progressive airway remodeling. We critically evaluate respiratory-adaptive nanocarrier systems, including polymer nanoparticles (PLGA-PEG) with 6.5-fold enhanced Neutrophil targeting efficiency (*p* < 0.001) and lipid nanoparticles (LNPs) achieving >90% siRNA-mediated inflammatory gene suppression. Despite advancements, clinical translation remains hindered by technical limitations in nanoparticle engineering, chronic pulmonary biocompatibility risks (eg, silica nanoparticles elevating TGF-β by 1.8-fold, *p* < 0.05), and stringent regulatory requirements. Future research must prioritize intelligent stimulus-responsive platforms for inflammation-triggered drug release, multidisease targeting nanotechnologies, and AI-driven patient-specific formulations. By integrating mechanistic insights with translational strategies, this work provides a roadmap to advance nano-interventions toward precision therapeutics for COPD.

This cross-sectional study is based on the NHANES (1999-2010) database and aims to explore the potential relationship between the CALLY index and stroke in the U.S. population. This cross-sectional study utilized data from NHANES (1999-2010), including 17,511 American participants after data cleaning. Laboratory markers related to the CALLY index were obtained through standardized biological sample collection and analysis procedures performed by trained professionals. Stroke status was determined based on self-reported questionnaires. Various statistical methods were employed to examine the association between the CALLY index and stroke, as well as its predictive efficacy for stroke risk, including multivariable logistic regression, subgroup analysis, RCS analysis, and ROC analysis. Among the 17,511 participants analyzed, our findings revealed a nonlinear L-shaped negative association between the CALLY index and stroke risk. In Model 3, a higher CALLY index was significantly associated with a lower stroke risk (OR: 0.99, 95% CI: 0.98-0.99, p = 0.045). Additionally, participants in the highest quartile (Q4) of the CALLY index had a 25% lower likelihood of stroke compared to those in the lowest quartile (Q1) (OR: 0.75, 95% CI: 0.58-0.97, p = 0.030). Furthermore, ROC analysis demonstrated that the CALLY index had superior predictive performance for stroke risk compared to the SIRI and SII indices. A reduced CALLY index may be linked to a higher risk of stroke. Furthermore, the CALLY index demonstrates superior predictive performance compared to the SIRI and SII indices. The association between the CALLY index and stroke risk provides valuable insights for future stroke prevention and management strategies.

Acne scarring is a common consequence of acne vulgaris. Recently, there have been huge advancements in photoelectric therapies for scarring, leading to a growing body of literature on the efficacy and safety of these devices. However, interventional studies are hindered by the absence of standardized and validated outcome measures for acne scarring. In this article, we aim to review current grading modalities to assist clinicians in conducting acne scar research and therapies. PubMed and MEDLINE online databases were searched to identify acne scarring severity measurement tools. Each was classified into objective tools, subjective investigator-reported or patient-reported assessments and they were evaluated for reliability, sensitivity, validity and other important aspects. Objective instruments for assessing clinical efficacy in acne scarring show promise, especially PRIMOS, a three-dimensional imager with strong interrater reliability [intraclass correlation coefficient (ICC) > 0.90] and intrarater reliability (ICC > 0.96). Regarding subjective assessments, the Échelle d'Évaluation Clinique des Cicatrices d'Acné (ECCA) tool features the widest range of applications and shows acceptable performance. The original ECCA tool scored five out of eight points, while the adapted version achieved six out of eight points after combining three essential factors: reliability, sensitivity and validity. The Goodman and Baron Global Acne Scarring Grading System (GSGS) score also achieved a good score of seven out of eight. However, most scales demonstrated poor or moderate performance owing to the lack of reliability testing and evidence from independent assessment. Our conclusion is that PRIMOS stands out as a strong objective tool, whereas GSGS and adapted ECCA are the leading subjective scales with acceptable to strong performance. More importantly, there is the need for standardized scales, facilitating the pooling of results for systematic reviews, meta-analyses and clinical recommendations.