Life sciences最新文献

{"title":"The role of FGF21 in the metabolic adjustments required for exercise capacity","authors":"Lisa Abe ,&nbsp;Robert Dantzer","doi":"10.1016/j.lfs.2025.123940","DOIUrl":"10.1016/j.lfs.2025.123940","url":null,"abstract":"<div><div>Fatigue is one of the most common and persistent symptoms experienced by patients with various medical conditions. It is characterized by its enduring nature, lack of improvement after a good night's sleep, and interference with daily functioning. The mechanisms behind fatigue remain controversial. In cancer patients, inflammation and mitochondrial dysfunction appear to be the predominant contributors. Mitochondrial dysfunction results from oxidative stress and inflammation. This condition leads to the production and release of soluble mediators known as mitokines, which act in an autocrine, paracrine, and endocrine manner to help the body adapt to the changes in energy metabolism caused by mitochondrial dysfunction. The main mitokines include growth differentiation factor (GDF) 15 and fibroblast growth factor (FGF) 21. We have already gathered evidence highlighting the pivotal role of GDF15 in the behavioral fatigue that arises in response to chemotherapy. In this perspective article, we explore whether the existing knowledge about the role of FGF21 in metabolic adaptations during cellular stress positions this mitokine as a potential candidate for cancer-related fatigue. To do this, we <strong>summarize</strong> how FGF21 is produced at the level of each organ involved in energy metabolism and how its local and distant effects may influence the capacity to engage in energy-intensive activities such as physical exercise.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123940"},"PeriodicalIF":5.1,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925010","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":"Dysregulation of the TNF-α-OTUD3-PPARγ signaling axis exacerbates retinal oxidative stress and inflammation in diabetic retinopathy","authors":"Jialin Zhang ,&nbsp;Zhen Wang ,&nbsp;Junjun Liu ,&nbsp;Wenchang Xu ,&nbsp;Lu Lu ,&nbsp;Na Zhou ,&nbsp;Yongfeng Song","doi":"10.1016/j.lfs.2025.123933","DOIUrl":"10.1016/j.lfs.2025.123933","url":null,"abstract":"<div><h3>Aims</h3><div>Diabetic retinopathy (DR) is one of the major complications of diabetes. In addition to hyperglycemia, various mechanisms contribute to the development of microvascular damage to the retina, which have not been fully elucidated. The aim of this study was to investigate Ovarian tumor domain-containing protein 3 (OTUD3)'s protection against DR by targeting peroxisome proliferator-activated receptor γ (PPARγ)-mediated dysfunction and identifying therapeutic strategies.</div></div><div><h3>Materials and methods</h3><div>We conducted clinical analysis of 208 type 2 diabetes mellitus (T2DM) patients with OTUD3 genotyping, combined with diabetic homozygous mutated (<em>Otud3</em>^{<em>−/−</em>}) mouse models and retinal pigment epithelium (RPE) cell lines (OTUD3 knockdown/mutation).</div></div><div><h3>Key findings</h3><div>We found increased hyperreflective foci (HRF) associated with an increased immune activation in diabetic <em>Otud3</em>^{<em>−/−</em>} mice compared to <em>Otud3</em> wild-type (<em>Otud3</em>^<em>+/+</em>) mice. OTUD3 knockdown or mutated cells showed increased cell dysfunction and oxidative stress markers under inflammatory conditions. Further upstream transcription factors predict analysis suggest PPARγ as the potential target of OTUD3. Finally, we found PPARγ agonist could rescue the phenotype in RPE cells characterized by increased ROS levels, enhanced migration, and elevated apoptosis resulting from OTUD3 loss of function through knockdown or mutation.</div></div><div><h3>Significance</h3><div>Our study offers novel insights into how deubiquitylase OTUD3 maintains the normal function of the retina by deubiquitylating PPARγ and provides a novel therapeutic target for this vision-threatening diabetic complications.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123933"},"PeriodicalIF":5.1,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933146","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":"Maternal obesogenic diet causes insulin resistance by modulating insulin signaling pathways in peripheral tissues of offspring: a systematic review","authors":"Carolina Ramos de Mendonça ,&nbsp;Lígia Cristina Monteiro Galindo ,&nbsp;Bruna Karoline Alves de Melo Silva ,&nbsp;Brenda Hilary Avelino de Vasconcelos ,&nbsp;Vitor Carlos de Araújo Bandeira ,&nbsp;Sandro Massao Hirabara ,&nbsp;Beatrice Morio ,&nbsp;Diogo Antonio Alves de Vasconcelos","doi":"10.1016/j.lfs.2025.123947","DOIUrl":"10.1016/j.lfs.2025.123947","url":null,"abstract":"<div><div>Overweight and obesity during critical periods, gestation and/or lactation, can harm offspring metabolic health. Maternal obesogenic diets may program offspring long-term, impairing physiology and increasing risk for insulin resistance. A key mechanism is the reduced expression/activity of insulin signaling proteins in peripheral glucose-metabolizing tissues. This systematic review examined the impact of maternal obesogenic diets on insulin resistance in the offspring of rats, through modulation of insulin signaling proteins in skeletal muscle, liver, and white adipose tissue. Searches in LILACS, PubMed, Web of Science, Scopus, and Sigle via Opera Gray yielded 2212 studies; 43 met inclusion criteria, following a PROSPERO-registered protocol. Findings showed reduced expression and activity of IRS-1, PI3K, AKT and GLUTs in peripheral tissues, alongside increased body weight, glucose intolerance, and insulin resistance. Thus, maternal obesogenic diets impair insulin signaling and related metabolic outcomes in offspring.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123947"},"PeriodicalIF":5.1,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933136","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":"CpG-mediated TLR9 signaling pathway enhances the efficacy of the OprF/PcrV DNA vaccine with cGAS-STING-activating properties","authors":"Linxia Tian,&nbsp;Hongxi He,&nbsp;Hanbai Liu,&nbsp;Yating Zhang,&nbsp;Xian Yu","doi":"10.1016/j.lfs.2025.123930","DOIUrl":"10.1016/j.lfs.2025.123930","url":null,"abstract":"<div><h3>Aims</h3><div>This study aimed to overcome the limited protective efficacy of the bivalent DNA vaccine (DNA-OprF/PcrV) against <em>Pseudomonas aeruginosa</em> (PA) infection by developing a complexed adjuvant strategy to enhance immunogenicity and protection, providing a novel clinical candidate vaccine.</div></div><div><h3>Materials and methods</h3><div>We formulated a bivalent DNA vaccine encoding PA antigens OprF and PcrV (DNA-OprF/PcrV) complexed with the TLR9 agonist CpG adjuvant (DNA-OprF/PcrV + CpG). In vitro mechanistic studies assessed synergistic pathway activation and dendritic cell maturation, while murine models evaluated humoral immunity (antibody titers), cellular immunity (Th1/CTL responses), and protective efficacy via pulmonary infection models with bacterial burden quantification and inflammation analysis.</div></div><div><h3>Key findings</h3><div>The CpG-adjuvanted vaccine synergistically activated both cGAS-STING (vaccine-mediated) and TLR9 (CpG-mediated) pathways, significantly enhancing dendritic cell maturation and innate immunity. Consequently, it amplified adaptive immunity, including potentiated Th1 polarization and cytotoxic T lymphocyte (CTL) activity alongside elevated PA-specific antibody titers. In pulmonary infection models, this formulation conferred superior protection marked by significantly reduced bacterial burden and attenuated inflammation compared to the non-adjuvanted vaccine.</div></div><div><h3>Significance</h3><div>This work demonstrates that the CpG-adjuvanted DNA vaccine complex overcomes DNA vaccine limitations through dual-pathway synergy, providing a clinically translatable strategy against multidrug-resistant PA infection and pioneering a cGAS-STING/TLR9 co-activation paradigm for antibacterial vaccine design.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"380 ","pages":"Article 123930"},"PeriodicalIF":5.1,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925009","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":"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}