Experimental gerontology最新文献

{"title":"UBE2N modulates osteoclast differentiation via BTK-PLCγ2-Ca2+ signaling pathway to promote osteoporosis","authors":"Yiqing Chen ,&nbsp;Ruixue Ying ,&nbsp;Liya Ai ,&nbsp;Fang Dai ,&nbsp;Qiu Zhang ,&nbsp;Ping Wang ,&nbsp;Fuhua Chen","doi":"10.1016/j.exger.2025.112751","DOIUrl":"10.1016/j.exger.2025.112751","url":null,"abstract":"<div><div>Osteoporosis is a prevalent public health issue and the underlying mechanism is an imbalance in bone remodeling. Excessive bone resorption caused by upregulation of osteoclast activity is a key factor in the pathogenesis of osteoporosis. Studies have shown that RNA binding protein (RBP) may play an important role in mechanism of OP through interaction with RNA. It has been reported that ubiquitin conjugating enzyme 2 N (UBE2N), as an RBP, is highly expressed in the clinical samples of osteoporotic patients. However, the role and mechanism of action of UBE2N in the regulation of osteoclast differentiation remain unclear. The aim of this study is to evaluate the effects and mechanisms of UBE2N in promoting osteoclastogenesis. In this study, we demonstrated that UBE2N is notably elevated in patients with osteoporosis. Furthermore, our findings revealed that the interference of UBE2N significantly improves osteoporosis of mice, and impedes osteoclast differentiation and bone resorption both in vitro and in vivo. To investigate the molecular mechanisms by which UBE2N influences osteoclast differentiation and bone resorption, we employed RNA sequencing to investigate its downstream related molecules and established that UBE2N regulated the expression of bruton tyrosine kinase (BTK). More importantly, we found that UBE2N may affect osteoclast differentiation and bone resorption by enhancing the expression of the p-BTK gene, which activates the phospholipase Cγ2 (PLCγ2)-Ca²⁺ signaling pathway. Based on these findings, our study highlights the potential of UBE2N as a promising therapeutic target for osteoporosis.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"204 ","pages":"Article 112751"},"PeriodicalIF":3.9,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143821254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age at menarche and risk of non-alcoholic fatty liver disease: Insights from the NHANES 2017–2020 and Mendelian randomization analyses","authors":"Guifei Si ,&nbsp;Xiaopan Lv ,&nbsp;Yuxin Ge ,&nbsp;Rui Zhang ,&nbsp;Dongxiao Hao ,&nbsp;Xuemei Chen ,&nbsp;Changchun Wang ,&nbsp;Yuquan Li ,&nbsp;Xiuping Li ,&nbsp;Xuemin Yuan","doi":"10.1016/j.exger.2025.112748","DOIUrl":"10.1016/j.exger.2025.112748","url":null,"abstract":"<div><h3>Background</h3><div>This study aimed to explore the causal relationship between age at menarche (AAM) and non-alcoholic fatty liver disease (NAFLD), leveraging data from the 2017–2020 National Health and Nutrition Examination Survey (NHANES) alongside Mendelian randomization (MR) analyses. Notably, this research represents the first attempt to link AAM to NAFLD using genetic methodologies, thereby providing novel insights into the interplay between these two conditions.</div></div><div><h3>Methods</h3><div>Cross-sectional data from 2730 participants were analyzed using logistic regression to evaluate the association between AAM and NAFLD risk. A two-sample MR study was performed to investigate causal relationships, utilizing genetic data from large-scale genome-wide association studies (GWASs). The inverse variance weighted (IVW) method served as the primary MR analysis approach.</div></div><div><h3>Results</h3><div>A significant negative association between AAM and NAFLD was found in Model 3 (OR = 0.85, 95 % CI: 0.74–0.97). Participants in the highest AAM quintile exhibited a 68 % reduction of NAFLD prevalence compared to those in the lowest AAM quintile (OR = 0.32, 95 % CI: 0.11–0.97). MR analysis confirmed a potential negative causal association (discovery: OR = 0.81, 95 % CI: 0.73–0.90; validation: OR = 0.80, 95 % CI: 0.66–0.96).</div></div><div><h3>Conclusions</h3><div>Our findings indicate a potential causal association between AAM and NAFLD, suggesting that early AAM may serve as a potential risk marker for NAFLD. This highlights the importance of incorporating AAM into clinical risk assessment tools and developing targeted prevention strategies for at-risk populations. Further research is needed to clarify the underlying mechanisms and to explore the potential benefits of early intervention.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"204 ","pages":"Article 112748"},"PeriodicalIF":3.9,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143790994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Balancing benefits and risks of aerobic exercise for aging and musculoskeletal health","authors":"Wenduo Liu ,&nbsp;Zilin Wang ,&nbsp;Yu Gu,&nbsp;Jae Cheol Kim,&nbsp;Sang Hyun Kim","doi":"10.1016/j.exger.2025.112747","DOIUrl":"10.1016/j.exger.2025.112747","url":null,"abstract":"<div><h3>Background</h3><div>Long-term exercise is recognized as one of the most effective means of maintaining health after aging, but the relationship between moderate exercise and health in the older population is often overlooked.</div></div><div><h3>Objective</h3><div>The present study was conducted to investigate the effects of excessive endurance exercise on the old mice musculoskeletal system.</div></div><div><h3>Results</h3><div>The 8 weeks of normal endurance exercise significantly improved skeletal muscle mitochondrial biogenesis and increased femoral osteogenesis in young and old mice. However, the continued accumulation of total exercise volume as the exercise cycle was prolonged resulted in the younger and older mice exhibiting different exercise effects. After 8–16 weeks of moderate-intensity endurance exercise, young mice showed consistent effects of increased mitochondrial biogenesis in skeletal muscle. However, after 12–16 weeks of moderate-intensity endurance exercise, the original effects of exercise-induced mitochondrial biosynthesis were instead impaired in older mice. After 16 weeks of exercise, the aged mice showed a produces consumptive weight loss, an increase inflammation level in adipose tissue, and a decrease in femoral bone mineral density. Interestingly, with an increase in total exercise, the level of skeletal muscle inflammation in old mice did not increase significantly, while a longer exercise cycle reduced the level of skeletal muscle apoptosis, thereby maintaining the state of skeletal muscle.</div></div><div><h3>Conclusions</h3><div>Appropriate moderate-intensity endurance exercise has a significant gain in maintaining musculoskeletal health in aged mice. However, excessive endurance impairs the health of the musculoskeletal system in aged mice.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"204 ","pages":"Article 112747"},"PeriodicalIF":3.9,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143759713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Bufexamac, a class IIb HDAC inhibitor, on behavior and neuropathological features in an Aβ-induced rat model of Alzheimer's disease","authors":"Monireh Mirehei ,&nbsp;Fereshteh Motamedi ,&nbsp;Nader Maghsoudi ,&nbsp;Zahra Mansouri ,&nbsp;Soudabeh Naderi ,&nbsp;Fariba Khodagholi ,&nbsp;Fatemeh Abbaszadeh","doi":"10.1016/j.exger.2025.112746","DOIUrl":"10.1016/j.exger.2025.112746","url":null,"abstract":"<div><div>It has been suggested that Alzheimer's disease (AD), a progressive neurological condition, can potentially be treated through epigenetic means by targeting histone deacetylases (HDACs), enzymes that regulate gene expression. In this study, we investigated the molecular mechanisms of Bufexamac, in an animal model of AD. Bufexamac specifically targets Class IIb HDACs, which are particularly relevant in the context of neuroinflammation and neurodegeneration. This selectivity may reduce off-target effects commonly associated with broader-spectrum HDAC inhibitors, such as pan-HDAC inhibitors, which can affect multiple HDAC classes and potentially lead to undesirable side effects. Male rats injected with Aβ_25–35 for AD-like symptoms were treated with 20 μg/rat Bufexamac for 8 days. Cognitive function, depression, and anxiety were assessed through behavioral tests, while Western blotting, H&amp;E staining, and ELISA were used to detect protein expression, morphological changes, and enzyme activity. Bufexamac treatment markedly improved cognitive and behavioral impairments in Aβ-injected rats and regulated the key proteins related to neuroinflammation (GFAP, Iba1), histone, and α-tubulin acetylation. Simultaneously, it decreased the expression of proteins in the stromal interaction molecule (STIM) pathway. Furthermore, Bufexamac lowered the activity of monoamine oxidase enzymes, elevated the count of healthy neurons, and ameliorated neuronal structure in the hippocampus. Overall, these findings suggest that Bufexamac could be a more targeted therapy for AD than other non-selective HDAC inhibitors, which often have diverse functions and potential side effects. Bufexamac enhances cognitive function and alleviates depression and anxiety by regulating proteins related to neuroinflammation, histone, and α-tubulin acetylation, as well as modulating STIM levels and MAO activity.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"204 ","pages":"Article 112746"},"PeriodicalIF":3.9,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miRNA and piRNA differential expression profiles in Alzheimer's disease: A potential source of pathology and tool for diagnosis","authors":"Benjamin Landon ,&nbsp;Kumudu Subasinghe ,&nbsp;Nathalie Sumien ,&nbsp;Nicole Phillips","doi":"10.1016/j.exger.2025.112745","DOIUrl":"10.1016/j.exger.2025.112745","url":null,"abstract":"<div><div>Alzheimer's Disease (AD) is the most prevalent form of dementia and one of the leading causes of death in the United States, and despite our best efforts and recent advancements, a treatment that stops or substantially slows its progression has remained elusive. Small extracellular vesicles (sEVs), hold the potential to alleviate some of the common issues in the field by serving to better differentiate AD and non-AD individuals. These vesicles could provide insights into therapeutic targets, and potentially an avenue towards early detection. We compared the sEV cargo profiles of AD and non-AD brains (<em>n</em> = 6) and identified significant differences in both the micro RNA (miRNA) and Piwi-interacting RNA (piRNA) cargo through sEV isolation from temporal cortex tissue, followed by small RNA sequencing, and differential expression analysis. Differentially expressed miRNAs targeting systems relevant to AD included miR-206, miR-4516, miR-219a-5p, and miR-486-5p. Significant piRNAs included piR-6,565,525, piR-2,947,194, piR-7,181,973, and piR-7,326,987. These targets warrant further study for their potential role in the progression of AD pathology by dysregulating cellular activity; additionally, future large-scale studies of neuronal sEV miRNA profiles may facilitate the development of diagnostic tools which can aid in clinical trial design and recruitment. Longitudinal analysis of sEV data, perhaps accessible through plasma surveyance, will help determine at what point these miRNA and/or piRNA profiles begin to diverge between AD and non-AD individuals.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"204 ","pages":"Article 112745"},"PeriodicalIF":3.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143759714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term prognostic value of CRP–albumin–lymphocyte index in elderly patients with heart failure with preserved ejection fraction","authors":"Qingwei He ,&nbsp;Yukun Cao ,&nbsp;Xingman Fan ,&nbsp;Bowen Li ,&nbsp;Qiongyi He ,&nbsp;Haitao Zhang","doi":"10.1016/j.exger.2025.112744","DOIUrl":"10.1016/j.exger.2025.112744","url":null,"abstract":"<div><h3>Background</h3><div>Heart failure with preserved ejection fraction (HFpEF) is a complex and heterogeneous clinical condition characterized by the interplay of malnutrition and immune inflammation, especially in elderly patients. The CRP-Albumin-Lymphocyte (CALLY) index, a novel composite indicator reflecting immune inflammation and nutritional status, has not yet been validated as a prognostic tool in elderly patients with HFpEF.</div></div><div><h3>Methods</h3><div>This retrospective study included 320 elderly patients hospitalized at the Air Force Medical Center from October 2016 to April 2019 due to HFpEF. Patients were stratified into the all-cause mortality and the survival groups according to follow-up outcomes. Kaplan–Meier analysis and Cox regression were performed to identify risk factors associated with poor prognosis. Additionally, we constructed and evaluated a nomogram based on the CALLY index to predict survival rates.</div></div><div><h3>Results</h3><div>During the follow-up period, 137 cases (42.81 %) of patients experienced all-cause mortality. Kaplan-Meier survival curves and Cox regression analysis revealed that a lower CALLY index (HR 0.811, 95 % CI 0.714–0.921, <em>P</em> = 0.001) was independently associated with adverse prognosis in elderly patients with HFpEF. The nomogram incorporating the CALLY index exhibited robust predictive performance for predicting 1-year, 3-year, and 5-year survival outcomes.</div></div><div><h3>Conclusion</h3><div>Our findings demonstrate that the CALLY index is an independent predictor of long-term mortality in elderly patients with HFpEF. The developed nomogram incorporating the CALLY index could effectively predict survival probabilities.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"204 ","pages":"Article 112744"},"PeriodicalIF":3.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143759716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Baicalin alleviates intervertebral disc degeneration by inhibiting the p38 MAPK signaling pathway","authors":"Yating Wu ,&nbsp;Fengrui Li ,&nbsp;Shibin Shu ,&nbsp;Zhenhua Feng ,&nbsp;Yong Qiu ,&nbsp;Sen Li ,&nbsp;Zezhang Zhu","doi":"10.1016/j.exger.2025.112743","DOIUrl":"10.1016/j.exger.2025.112743","url":null,"abstract":"<div><h3>Background</h3><div>Intervertebral disc degeneration (IVDD) represents a prevalent degenerative pathology of the spinal, primarily precipitated by inflammatory processes and the deterioration of extracellular matrix (ECM). Baicalin has an effective anti-inflammatory effect on degenerative diseases. In addition, the P38 mitogen-activated protein kinase (MAPK) signaling pathway plays a crucial role in the pathogenesis of IVDD.</div></div><div><h3>Objective</h3><div>To investigate the therapeutic potential of baicalin in modulating pathological changes in IVDD.</div></div><div><h3>Methods</h3><div>To design an in vitro model of degeneration of nucleus pulposus cells (NPCs) stimulated by IL-1β and an in vivo mouse model of needling to assess the protective effect of baicalin against IVDD and its underlying mechanism.</div></div><div><h3>Results</h3><div>Baicalin down-regulated inflammatory factors (INOS, COX-2, IL-6) and catabolic factors (MMP-3, MMP-13, ADAMTS-5) while up-regulating anabolic factors (collagen II, SOX-9) by inhibiting the activation of the p38 MAPK signaling pathway, in addition to slowing down the progression of IVDD in the mouse acupuncture model.</div></div><div><h3>Conclusion</h3><div>Our study demonstrated in vitro experiments that baicalin attenuates IL-1β-stimulated IVDD by inhibiting activation of the P38 MAPK signaling pathway. Meanwhile, the effects of baicalin were also confirmed in vivo experiments, Consequently, we propose that baicalin is a promising therapeutic agent for the treatment of disc degeneration.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"204 ","pages":"Article 112743"},"PeriodicalIF":3.9,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143775111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of blood ethylene oxide levels with osteoarthritis and rheumatoid arthritis: Evidence from NHANES (2013–2020)","authors":"Zhaoyi Fang ,&nbsp;Qingxiang Hu ,&nbsp;Wenxin Liu","doi":"10.1016/j.exger.2025.112739","DOIUrl":"10.1016/j.exger.2025.112739","url":null,"abstract":"<div><h3>Objectives</h3><div>Osteoarthritis (OA) and rheumatoid arthritis (RA) are common conditions with important public health implications. The role of environmental toxins in their pathogenesis is increasingly recognized; however, the impact of ethylene oxide (EO) exposure on OA and RA remains unexplored. This study investigated the association between blood EO levels and the prevalence of OA and RA in the US population, using data from the National Health and Nutrition Examination Survey (NHANES) 2013–2020.</div></div><div><h3>Methods</h3><div>NHANES 2013–2020 participants ≥40 years old with OA or RA who reported the condition during the NHANES interview were included. Blood EO levels were directly measured using hemoglobin adduct quantification. Univariate and multivariable logistic regression models were used to evaluate the association between EO exposure and OA and RA, adjusting for potential confounders. Restricted cubic spline (RCS) analysis was performed to assess potential non-linear relations.</div></div><div><h3>Results</h3><div>A total of 3476 participants (mean age: 60.0 years; 52.0 % female) were included in the study. In the unadjusted model, participants in the highest EO quintile did not have a significantly higher likelihood of OA (odds ratio [OR] = 1.23; 95 % confidence interval [CI]: 0.86–1.74) or RA (OR = 1.58; 95 % CI: 0.97–2.58) compared to those in the lowest quintile. However, after adjustment, participants in the highest EO quintile had significantly greater likelihood of having OA (aOR = 2.00; 95 % CI: 1.30–3.07) and RA (aOR = 1.81; 95 % CI: 1.08–3.03) compared to those in the lowest quintile. RCS analyses suggested no significant non-linear associations between EO exposure and OA or RA.</div></div><div><h3>Conclusion</h3><div>This study identified independent associations between EO exposures and an increased prevalence of OA and RA. These findings highlight the need for regulatory measures to minimize EO exposure and further investigations to confirm causal relationships.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"204 ","pages":"Article 112739"},"PeriodicalIF":3.9,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143715260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Mesencephalic astrocyte-derived neurotrophic factor alleviated 6-OHDA-induced cell damage via ROS-AMPK/mTOR mediated autophagic inhibition” [Exp. Gerontol. Volume 89 (2017), 45–56]","authors":"Jingxing Zhang ,&nbsp;Qiong Cai ,&nbsp;Ming Jiang ,&nbsp;Yigang Liu ,&nbsp;Hua Gu ,&nbsp;Jia Guo ,&nbsp;Hui Sun ,&nbsp;Jianmin Fang ,&nbsp;Lingjing Jin","doi":"10.1016/j.exger.2025.112733","DOIUrl":"10.1016/j.exger.2025.112733","url":null,"abstract":"","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"203 ","pages":"Article 112733"},"PeriodicalIF":3.9,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanism of melatonin-mediated mitophagy regulating proline production to ameliorate skin aging","authors":"Tao Quan,&nbsp;Ran Li,&nbsp;Ting Gao","doi":"10.1016/j.exger.2025.112738","DOIUrl":"10.1016/j.exger.2025.112738","url":null,"abstract":"<div><div>Collagen loss is one of the major contributor to signs of skin aging such as dryness, roughness, and wrinkle formation, which is closely linked to a decline in the amount of proline produced in mitochondria. Melatonin has been shown to improve several clinical signs of skin aging, while the mechanism is unclear. In our study, we found that mitophagy, proline synthesis key enzyme NADK2 and proline and collagen levels were significantly reduced, while oxidative stress levels increased in aging skin, and melatonin supplementation could effectively up-regulate mitophagy level and restore proline synthesis and further improved skin aging. However, proline supplementation could also exert an anti-aging effect, while it had no effect on the mitochondrial dysfunction. Moreover, our study indicated that melatonin enters the cell by binding to the MT1 receptor and then enters the mitochondria via the PEPT1 transporter to exert its mitochondrial protective effects. This study helps to elucidate the mechanism of mitochondrial dysfunction-induced skin aging, and provides new theoretical guidance for revealing the mechanism of skin aging and rationally utilizing endocrine hormones to improve skin aging, which has a broad application prospect.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"204 ","pages":"Article 112738"},"PeriodicalIF":3.9,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143705026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}