Life sciences最新文献

{"title":"New role of obscure acylation modifications in cardiovascular diseases: what's beyond?","authors":"Zhongyi Zhang ,&nbsp;Wei Hu ,&nbsp;Qian Ding ,&nbsp;Yi Zhun Zhu","doi":"10.1016/j.lfs.2025.123944","DOIUrl":"10.1016/j.lfs.2025.123944","url":null,"abstract":"<div><div>Cardiovascular diseases remain the leading cause of global mortality, yet their molecular mechanisms are incompletely understood. Recent advances highlight the critical role of obscure acylation modifications in regulating cardiac homeostasis and disease pathogenesis, such as succinylation, crotonylation, malonylation, β-hydroxybutyrylation, and lactylation. These post-translational modifications serve as metabolic sensors, dynamically linking cellular metabolism to epigenetic and functional changes in proteins. This mini-review synthesizes emerging evidence on how dysregulated obscure acylations contribute to cardiovascular diseases, including heart failure, ischemic injury, and atherosclerosis, by altering mitochondrial function, gene expression, or cellular signaling. We further discuss the therapeutic potential of targeting acyl-modifying enzymes and innovative strategies like machine learning for modification prediction. Despite technological challenges in profiling rare modifications, this field offers promising avenues for novel biomarkers and precision therapies. By elucidating the relationship between cardiovascular pathologies and obscure acylation modifications, this mini-review aims to inspire future research for clinical intervention of cardiovascular diseases.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123944"},"PeriodicalIF":5.1,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A PBX1-IL7R axis mediates liver fibrosis in non-alcoholic fatty liver disease","authors":"Zhen Yang ,&nbsp;Jinbo Zhang ,&nbsp;Qihang Wang ,&nbsp;Huihui Xu ,&nbsp;Xihu Qin ,&nbsp;Fangqiao Lv","doi":"10.1016/j.lfs.2025.123948","DOIUrl":"10.1016/j.lfs.2025.123948","url":null,"abstract":"<div><h3>Aims</h3><div>Non-alcoholic fatty liver disease (NAFLD), also known as metabolic dysfunction associated steatotic liver disease (MASLD), represents a spectrum of chronic liver diseases that eventually lead to cirrhosis and hepatocellular carcinoma. Liver fibrosis is both a pathological feature and a contributing factor in NAFLD. In the present study we investigated whether targeting pre-B cell leukemia transcription factor 1 (PBX1) and interleukin 7 receptor (IL7R) might ameliorate liver fibrosis in the context of NAFLD.</div></div><div><h3>Methods and materials</h3><div>NAFLD was induced in C57/B6j mice by feeding with a choline-deficient amino acid defined high-fat diet (CDAA-HFD).</div></div><div><h3>Key findings</h3><div>Both PBX1 expression and IL7R expression were up-regulated in hepatic stellate cells (HSCs) isolated from the mice fed the CDAA-HFD compared to those isolated from the control mice. Myofibroblast-specific PBX1 depletion, by injecting the mice with AAV6 carrying short-hairpin RNA (shRNA) against PBX1, significantly attenuated liver fibrosis induced by CDAA-HFD feeding. Similarly, myofibroblast-specific IL7R depletion significantly mitigated NAFLD-associated liver fibrosis. Of note, liver injury and steatosis were not influenced by either PBX1 or IL7R depletion. Importantly, IL7R blockade with a neutralizing antibody likewise diminished NAFLD-associated liver fibrosis. Finally, a positive correlation between PBX1 expression, IL7R expression, and myofibroblast activation was identified in liver specimens from NAFLD patients.</div></div><div><h3>Significance</h3><div>Our data demonstrate the feasibility of targeting the PBX1-IL7R axis for the intervention of NAFLD-associated liver fibrosis.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123948"},"PeriodicalIF":5.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144959393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of ferroptosis in doxorubicin-induced cardiotoxicity – An update","authors":"Pammi Bhadra ,&nbsp;Prisha Yadav ,&nbsp;Sanjot Kaur ,&nbsp;Padmini Topinar Hanumantharayudu,&nbsp;Sankarganesh Arunachalam","doi":"10.1016/j.lfs.2025.123945","DOIUrl":"10.1016/j.lfs.2025.123945","url":null,"abstract":"<div><div>Doxorubicin is a chemotherapeutic drug used in the treatment of a variety of cancers, such as cancer of the blood, bladder, breast, lymph system, stomach, neuroblasts, etc. Currently, its potential is severely limited as it leads to cardiotoxicity, a fatal side effect. Several studies have been carried out in the past few decades to elucidate the molecular mechanisms of this Doxorubicin-induced cardiotoxicity. This study aims to analyse the role of ferroptosis in the mechanism of Doxorubicin-induced cardiotoxicity, an area which remains comparatively unexplored. The article elaborates on the molecular pathogenesis of ferroptosis and the role of doxorubicin in triggering the same. Several biological pathways, especially Nrf2 (Nuclear factor erythroid 2-related factor 2)-mediated pathways, are influenced by doxorubicin, leading to ferroptosis. The study of molecular mechanisms of doxorubicin-induced cardiotoxicity is instrumental for developing therapeutic interventions that alleviate cardiotoxicity and improve the outcomes of doxorubicin usage, such as targeting ferritinophagy, which is one of the key factors in causing ferroptosis, and can reduce cardiotoxicity and can be a potential therapeutic strategy.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123945"},"PeriodicalIF":5.1,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of actions of the novel gabapentinoid drug mirogabalin on painful bladder hypersensitivity in rats with lipopolysaccharide-induced chronic cystitis","authors":"Masaru Yoshizumi ,&nbsp;Yutaka Kitano ,&nbsp;Chizuko Watanabe ,&nbsp;Shinobu Sakurada ,&nbsp;Hirokazu Mizoguchi","doi":"10.1016/j.lfs.2025.123942","DOIUrl":"10.1016/j.lfs.2025.123942","url":null,"abstract":"<div><h3>Aims</h3><div>Gabapentin reduces bladder pain and overactivity in lipopolysaccharide (LPS)-induced chronic cystitis in a rat model. This study evaluated the role of the spinal cord and the descending noradrenergic pathway in the effects of mirogabalin (MGB), a novel gabapentinoid drug on painful bladder hypersensitivity in this model.</div></div><div><h3>Main methods</h3><div>Chronic cystitis was induced in female Sprague–Dawley rats via repeated intravesical LPS instillation. von Frey filaments and continuous cystometry were used to assess bladder pain-related behaviors and micturition function, respectively. Changes in voltage-gated calcium channel α₂δ-1 subunits expression in the spinal dorsal horn (SDH) and locus coeruleus (LC) were analyzed using western blotting. Gabapentinoid effects were evaluated after systemic, intracerebroventricular, and intrathecal administration. Additionally, rats were treated with <em>N</em>-(2-chloroethyl)-<em>N</em>-ethyl-2-bromobenzylamine (DSP-4) to deplete noradrenergic nerves, in order to investigate the involvement of the descending noradrenergic system in the LC.</div></div><div><h3>Key findings</h3><div>MGB, as well as other gabapentinoids, reduced LPS-induced increases in cystitis-related pain and voiding frequency after systemic, intrathecal, or intracerebroventricular administration. Notably, MGB exhibited longer-lasting analgesic effects than other gabapentinoids. LPS-induced cystitis rats showed up-regulation of the α₂δ-1 subunit in the SDH and LC. Pretreatment with DSP-4 reversed the analgesic effects of gabapentinoids but did not affect their inhibitory effect on micturition.</div></div><div><h3>Significance</h3><div>The therapeutic effects of MGB in hypersensitivity associated with cystitis, similar to other gabapentinoids, are mediated by spinal and supraspinal actions, likely via the α₂δ-1 subunit. Additionally, MGB exerts its analgesic effects through a supraspinal mechanism via the descending noradrenergic pathway, whereas a different mechanism regulates micturition.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123942"},"PeriodicalIF":5.1,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EdgeNeXt-SEDP for cervical adenocarcinoma HPV-associated and non-HPV-associated diagnosis and decision support","authors":"Qi Chen ,&nbsp;Hao Wang ,&nbsp;Hao Zhang ,&nbsp;Zhenkun Zhu ,&nbsp;Xi Wei","doi":"10.1016/j.lfs.2025.123931","DOIUrl":"10.1016/j.lfs.2025.123931","url":null,"abstract":"<div><h3>Aims</h3><div>Adenocarcinoma of the uterine cervix exhibits substantial biological and histological heterogeneity, with subtype-specific differences in prognosis and therapeutic response. Conventional classification—based on histopathology, immunohistochemistry, and molecular testing—remains subjective, labor-intensive, and challenging to standardize. This study introduces EdgeNeXt-SEDP, a lightweight deep-learning framework for automated differentiation of HPV-associated (HPVA) and non-HPV-associated (NHPVA) subtypes from histopathological whole-slide images (WSIs).</div></div><div><h3>Materials and methods</h3><div>EdgeNeXt-SEDP integrates three synergistic components: a Squeeze-and-Excitation (SE) module to recalibrate channel-wise feature importance, dual-pooling feature fusion to enrich spatial representation, and progressive stochastic depth decay to enhance generalization. The model was trained and evaluated on 49 WSIs from 21 patients using standardized preprocessing, augmentation, and evaluation protocols. Performance metrics included accuracy, precision, specificity, and macro-averaged F1 score, benchmarked against DilateFormer, RepVIT, and EdgeNeXt architectures.</div></div><div><h3>Key findings</h3><div>EdgeNeXt-SEDP achieved 97.63% accuracy, 97.61% precision, 96.98% specificity, and a 97.58% macro-averaged F1 score, while maintaining computational efficiency with 1.9M parameters and 0.2G FLOPs. Ablation analyses confirmed that each module significantly contributed to performance, with the SE module yielding the largest gains. The proposed model consistently surpassed baseline methods without incurring additional computational cost.</div></div><div><h3>Significance</h3><div>By delivering high diagnostic accuracy in an efficient architecture, EdgeNeXt-SEDP offers a scalable and reliable solution for reducing interobserver variability and facilitating timely, individualized management of cervical adenocarcinoma. Its compact design supports integration into diverse clinical and resource-limited settings, advancing the application of AI in digital pathology.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123931"},"PeriodicalIF":5.1,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone acetylation: A key regulator of inflammatory responses","authors":"Siqi Gao ,&nbsp;Hua Xiao ,&nbsp;Haodang Luo ,&nbsp;Xiaoqian Tang ,&nbsp;Yanhua Zeng","doi":"10.1016/j.lfs.2025.123936","DOIUrl":"10.1016/j.lfs.2025.123936","url":null,"abstract":"<div><div>Histone acetylation is a critical epigenetic modification that influences several biological processes by altering chromatin structure and regulating gene expression, including chromatin remodeling, DNA replication, transcriptional regulation, signal transduction, autophagy, differentiation, and inflammatory responses. In eukaryotic cells, it ranks as one of the most common posttranslational modifications of histones and the earliest confirmed important positive transcriptional regulators. This review discusses the regulation of histone acetylation on the inflammatory response and comprehensively introduces the influence of histone acetylation on inflammation-related signaling pathways, pathogen infection, and inflammatory diseases. It is expected that this will provide new ideas and insights for the further development and application of histone acetylation inhibitors as therapeutic targets for inflammatory diseases.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123936"},"PeriodicalIF":5.1,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144903505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crosstalk between macrophages and diverse immune cells accelerates the development of acute lung injury","authors":"Hong-Kai Huang ,&nbsp;Shu-Pei Liu ,&nbsp;Xiao Deng ,&nbsp;Rui-Lin Zhao ,&nbsp;Yue Feng ,&nbsp;Jia-Si Wu","doi":"10.1016/j.lfs.2025.123925","DOIUrl":"10.1016/j.lfs.2025.123925","url":null,"abstract":"<div><div>Acute lung injury (ALI) is a severe pulmonary condition characterized by a high mortality rate. Its pathogenesis is complex, involving intricate interactions among various immune cells. Macrophages, as central players in the immune system, are critically involved in the onset, progression, and outcome of ALI. Extensive evidence demonstrates that macrophages engage in crosstalk with immune cells such as lymphocytes, neutrophils, and dendritic cells (DCs). Macrophages affect the recruitment, activation, and function of these immune cells through the secretion of cytokines, chemokines, and the expression of cell surface molecules. This influence thereby exacerbates the inflammatory response in ALI. A comprehensive understanding of how macrophages communicate with other immune cells helps us better understand how ALI develops. And this understanding also provides a theoretical basis for creating new immunotherapeutic methods. In this review, a systematic search was conducted using the keywords ‘ALI, macrophages, T cells, neutrophils, dendritic cells, intercellular crosstalk, immune function’ across six databases, including PubMed, SCI, CNKI, Wanfang Medicine, VIP Database, and X-MOL, covering literature from 2005 to 2024. Over 50 relevant studies were retrieved and reviewed, focusing on the crosstalk between macrophages and T cells, neutrophils, and dendritic cells (DCs) in the regulation of ALI, aiming to elucidate how these interactions contribute to ALI development.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123925"},"PeriodicalIF":5.1,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144908044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tripterygium glycoside tablet induces male reproductive toxicity in CIA rats by inhibiting the NELL2-Lumicrine system","authors":"Li Guo,&nbsp;Siqi Li,&nbsp;Zehui Li,&nbsp;Yuan Li,&nbsp;Jiashan Li,&nbsp;Huiting Cheng,&nbsp;Yuan Lu,&nbsp;Na Lin,&nbsp;Ying Xu","doi":"10.1016/j.lfs.2025.123935","DOIUrl":"10.1016/j.lfs.2025.123935","url":null,"abstract":"<div><h3>Aims</h3><div>Tripterygium glycoside tablet (TGT), a first-line anti-inflammatory drug for rheumatoid arthritis (RA), is severely limited in clinical use by male reproductive toxicity with unclear mechanisms. This study aimed to confirm TGT's anti-RA efficacy, characterize its reproductive toxicity in collagen-induced arthritis (CIA) rats, and elucidate whether the NELL2-Lumicrine system mediates such damage.</div></div><div><h3>Materials and methods</h3><div>TGT's anti-inflammatory efficacy in CIA rats was evaluated via arthritis scoring, histopathology, and cytokine quantification. Male reproductive toxicity was assessed using sperm analysis, fertilization evaluation, histopathology, and hormone measurement. NELL2-Lumicrine system targets were identified by immunofluorescence and Western blot. Integrated metabolomic and transcriptomic analyses explored TGT's effects on testicular metabolism and gene expression. Molecular docking, dynamics simulation, and cell co-culture experiments verified inhibitory effects of TGT's bioactive components on the NELL2-Lumicrine system.</div></div><div><h3>Key findings</h3><div>TGT alleviated joint swelling, reduced arthritis scores, and decreased serum TNF-α/IL-1β in CIA rats. However, TGT impaired sperm quality and fertilization capacity, increased sperm/embryo abnormalities, and induced testicular-epididymal damage, with hypothalamic-pituitary-gonadal axis hormone dysregulation. Mechanistically, TGT downregulated NELL2 and downstream targets (ROS1, OVCH2, ADAM28, ADAM3), disrupting sperm maturation. Multi-omics revealed TGT disrupted testicular steroid biosynthesis and Fgf signaling linked to the NELL2-Lumicrine system. Computational modeling and in vitro experiments confirmed triptolide and triptonide bind NELL2 strongly, suppressing its signaling pathway.</div></div><div><h3>Significance</h3><div>Our data provide the first evidence that TGT induces male reproductive toxicity by inhibiting the NELL2-Lumicrine system, downregulating NELL2 and its downstream targets (ROS1, OVCH2, ADAM28, and ADAM3), which are essential for sperm maturation.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123935"},"PeriodicalIF":5.1,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144913832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From synaptic dynamics to cognitive decline: Molecular insights into neuroplasticity","authors":"Basavaraju K C ,&nbsp;Poornima Priyadarshini","doi":"10.1016/j.lfs.2025.123937","DOIUrl":"10.1016/j.lfs.2025.123937","url":null,"abstract":"<div><div>Neuroplasticity, the nervous system's ability to adapt its activity in response to internal and external stimuli. This adaptability depends on activity-dependent mechanisms that alter the strength and efficiency of synaptic transmission. The key processes include neurotransmitter release, calcium ion influx, magnesium ion removal from <em>N</em>-methyl-<span>d</span>-aspartate (NMDA) receptors, trafficking of α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors, and complex intracellular signaling pathways. Glial cells and autophagic processes further contribute to the maintenance and regulation of synaptic plasticity. These mechanisms are pivotal for stabilizing synaptic connections and mitigating memory loss in neurological conditions such as Alzheimer's disease (AD). At the molecular level, synaptic plasticity involves an intricate network of proteins, receptors, and post-translational modifications that interact within coordinated signaling pathways to ensure structural and functional stability. Thus, any disruption in these mechanisms significantly contributes to the pathogenesis of various neurological disorders, including schizophrenia, depression, AD, and dementia. In this review, we explore the key molecular pathways that contribute to synaptic plasticity, ultimately aiming to understand disease pathology and related key targets for therapeutic interventions and disease prevention.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123937"},"PeriodicalIF":5.1,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Substituted 2-pyrrolinone compounds as inhibitors of B-cell activating factor (BAFF) for autoimmune diseases treatment","authors":"Stefania Olla ,&nbsp;Maria Laura Idda ,&nbsp;Manila Deiana ,&nbsp;Valeria Lodde ,&nbsp;Giuseppe Delogu ,&nbsp;Antonio Cristian Caria ,&nbsp;Matteo Floris ,&nbsp;Francesco Cucca","doi":"10.1016/j.lfs.2025.123938","DOIUrl":"10.1016/j.lfs.2025.123938","url":null,"abstract":"<div><div>B-cell activating factor (BAFF) is a cytokine that plays a critical role in the proliferation and differentiation of B cells. We have previously demonstrated that its inherited overexpression is associated with increased circulating B cell and immunoglobulin levels, correlating with increased risk of multiple sclerosis and systemic lupus erythematosus. These findings suggest that enhanced BAFF expression may be involved in the causal biology of these disorders, thus supporting the rationale for therapeutic inhibition of this cytokine. However, to date, no small-molecule modulator capable of inhibiting BAFF is available. We therefore employed a virtual screening approach to analyze a library of 275,561 small molecules, followed by in vitro validation of 218 selected compounds with potential to disrupt the interaction between BAFF and its receptor BAFFR. Our results identified two promising small molecules, C45 and C145, belonging to the substituted 2-pyrrolinone family, which effectively inhibited BAFF activity. These compounds warrant further investigation as potential therapeutic agents for BAFF-driven autoimmune diseases.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123938"},"PeriodicalIF":5.1,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}