Life sciences最新文献

{"title":"The emerging role of decorin in pancreatic islet biology: From development to degeneration","authors":"Huanjing Bi ,&nbsp;Ruiyang Ma ,&nbsp;Zuhan Chen ,&nbsp;Yang Li ,&nbsp;Xiaoming Ding","doi":"10.1016/j.lfs.2025.124185","DOIUrl":"10.1016/j.lfs.2025.124185","url":null,"abstract":"<div><div>Decorin, a small leucine-rich proteoglycan, has emerged as a multifunctional signaling molecule with critical implications for pancreatic islet biology beyond its canonical role in extracellular matrix organization. Despite extensive characterization of decorin's functions in matrix architecture and growth factor sequestration across various tissues, its specific contributions to pancreatic islet development and homeostasis remain insufficiently explored. Current evidence demonstrates decorin's molecular structure and post-translational modifications enable modulation of signaling pathways through pan-receptor tyrosine kinase inhibition and transforming growth factor-beta sequestration, with regulatory activities that vary substantially across distinct cellular and pathological environments. Within the pancreatic islet microenvironment, decorin influences pancreatic islet morphogenesis and beta-cell differentiation through modulation of local matrix composition and growth factor bioavailability, while conferring protection against diabetic complications through anti-fibrotic properties that mitigate peri-islet extracellular matrix remodeling observed in progressive islet dysfunction. By synthesizing findings from developmental biology, matrix biochemistry, and diabetes research, we address this critical knowledge gap and position decorin as an underrecognized regulator of pancreatic islet biology whose multifaceted mechanisms warrant investigation to reveal therapeutic strategies for preserving beta-cell function and preventing diabetes-associated fibrotic pathology.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"387 ","pages":"Article 124185"},"PeriodicalIF":5.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145896694","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":"Retraction notice to “Baicalin may alleviate inflammatory infiltration in dextran sodium sulfate-induced chronic ulcerative colitis via inhibiting IL-33 expression” [Life Sci. 186 (2017) 125–132]","authors":"Cheng-Liang Zhang ,&nbsp;Si Zhang ,&nbsp;Wen-Xi He ,&nbsp;Jing-Li Lu ,&nbsp;Yan-Jiao Xu ,&nbsp;Jin-Yu Yang ,&nbsp;Dong Liu","doi":"10.1016/j.lfs.2025.124177","DOIUrl":"10.1016/j.lfs.2025.124177","url":null,"abstract":"","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"386 ","pages":"Article 124177"},"PeriodicalIF":5.1,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145878687","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":"Retraction notice to “A novel approach to bladder dysfunction induced by bladder outlet obstruction: Low-intensity extracorporeal shock wave therapy promotes bladder regeneration” [Life Sci. 378 (2025) 123799]","authors":"Sheng-Tang Wu ,&nbsp;Tai-Jui Juan ,&nbsp;Jian-He Lu ,&nbsp;Kuang-Shun Chueh ,&nbsp;Jing-Wen Mao ,&nbsp;Cheng-Yu Long ,&nbsp;Shu-Mien Chuang ,&nbsp;Mei-Chen Shen ,&nbsp;Ting-Wei Sun ,&nbsp;Chiang-Ting Wang ,&nbsp;Yung-Shun Juan","doi":"10.1016/j.lfs.2025.124178","DOIUrl":"10.1016/j.lfs.2025.124178","url":null,"abstract":"","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"387 ","pages":"Article 124178"},"PeriodicalIF":5.1,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145878616","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":"Advances in AI for predicting pharmacological properties of natural medicines","authors":"Tianyu Xu ,&nbsp;Yuemiao Xu ,&nbsp;Jinger Zhang ,&nbsp;Yuchen Zhou ,&nbsp;Huiying Feng ,&nbsp;Aiqin Zhang ,&nbsp;Yuhua Zhang","doi":"10.1016/j.lfs.2025.124180","DOIUrl":"10.1016/j.lfs.2025.124180","url":null,"abstract":"<div><div>Artificial intelligence (AI), which includes machine learning (ML) and deep learning (DL), has become an important tool in drug development. An increasing number of studies have discovered pharmacologically active compounds in natural products, and AI's high-throughput capabilities have accelerated the drug discovery process. In the development of natural medicines, AI can use existing datasets and experimental data to screen for lead compounds with potential activity and predict disease-associated drug targets. Furthermore, using AI to predict the absorption, distribution, metabolism, excretion, and toxicity (ADMET) properties of lead compounds early in the drug discovery process can save time and money. This review introduces AI applications for predicting the pharmacological properties of natural drugs by outlining model construction principles and recent advances, summarizing key aspects such as feature selection and evaluation metrics, and discussing natural drug development challenges and opportunities.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"387 ","pages":"Article 124180"},"PeriodicalIF":5.1,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847719","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":"Adiponectin receptor agonist, AdipoRon, reduces the growth of prostate cancer cells and patient-derived organoids","authors":"Francielle C. Mosele ,&nbsp;Ana Luiza Romano Gabriel ,&nbsp;Nilton José dos Santos ,&nbsp;Caroline Nascimento Barquilha ,&nbsp;Caio Cesar Damasceno Monção ,&nbsp;Micheli Canuto de Lima ,&nbsp;Mark A. Rubin ,&nbsp;Sérgio Luis Felisbino ,&nbsp;Joanna Triscott","doi":"10.1016/j.lfs.2025.124175","DOIUrl":"10.1016/j.lfs.2025.124175","url":null,"abstract":"<div><div>Low adiponectin levels in obese men are associated with an incidence of aggressive prostate cancer (PCa). Despite significant advances in PCa treatment, some cases become resistant, making the development of new therapies crucial. An alternative treatment is the use of agonists, such as AdipoRon. Here, we elucidate the antitumor effects of AdipoRon on PCa models and demonstrate reduced cell proliferation, migration, and invasion in vitro. AdipoRon impaired mitochondrial respiration of androgen-dependent and castration-resistant cells. We show that this agonist reduces AR and PSA expression in androgen-dependent prostate cells. Adiponectin receptors (AdipoR1 and AdipoR2) were upregulated in PC3 and DU-145 cells. We hypothesize that the alteration of PPAR alpha could explain the effects of AdipoRon. Additionally, the antigrowth effects of AdipoRon were observed in the patient-derived organoids PM154 and MSK-PCa16. Our findings reveal that AdipoRon has strong in vitro antitumor effects on PCa, supporting its potential as a promising therapeutic candidate. Future studies should focus on in vivo models to validate these effects and explore the underlying mechanisms, which may open new therapies for PCa.</div></div><div><h3>Statement of implication</h3><div>AdipoRon decreases prostate cancer cell growth.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"387 ","pages":"Article 124175"},"PeriodicalIF":5.1,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145850239","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":"Adventitial fibroblast-derived NAMPT is associated with vascular remodeling in erythropoietin-induced abdominal aortic aneurysm","authors":"Xinyi Lyu ,&nbsp;Shuqin Ding ,&nbsp;Chongqing Jiang ,&nbsp;Yile Zhou ,&nbsp;Jiahao Shi ,&nbsp;Qi Liu ,&nbsp;Yajun Chen ,&nbsp;Xianpeng Dai","doi":"10.1016/j.lfs.2025.124179","DOIUrl":"10.1016/j.lfs.2025.124179","url":null,"abstract":"<div><div>Abdominal aortic aneurysm (AAA) remains a life-threatening condition with limited pharmacological interventions. While erythropoietin (EPO) has been implicated in AAA pathogenesis, its cell-type-specific effects on nicotinamide phosphoribosyltransferase (NAMPT)-mediated vascular remodeling remain unexplored. This study demonstrates that EPO administration in mice significantly induces AAA formation, characterized by aortic dilation, straightening of elastic laminae, and adventitial thickening. Through integrated in vivo and in vitro analyses, we identified that EPO differentially regulates NAMPT expression across vascular cell types: downregulating it in endothelial cells while robustly upregulating it in adventitial fibroblasts and infiltrating macrophages. Notably, EPO promoted proliferation of adventitial fibroblasts but suppressed endothelial cell growth. Mechanistically, the vascular adventitia emerged as the primary locus of NAMPT-driven pathology, where fibroblast-derived NAMPT creates a pro-inflammatory and pro-remodeling niche. These findings reveal a previously unrecognized role of adventitial fibroblasts in EPO-induced AAA through NAMPT dysregulation, suggesting novel therapeutic targets for AAA treatment. The study shifts therapeutic focus toward the adventitia as a key regulator of AAA progression.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"386 ","pages":"Article 124179"},"PeriodicalIF":5.1,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145850279","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":"O-GlcNAcylation stabilizes c-MYC to upregulate xCT and inhibit ferroptosis in ovarian cancer","authors":"Ying Tang ,&nbsp;Yaru Zhang ,&nbsp;Xinmei Chen ,&nbsp;Xiaotong Li ,&nbsp;Jingyuan Pei ,&nbsp;Ao Wang ,&nbsp;Zhengqing Luo ,&nbsp;Hongshuo Zhang ,&nbsp;Tonghui Ma ,&nbsp;Jianhui Fan ,&nbsp;Ying Kong","doi":"10.1016/j.lfs.2025.124172","DOIUrl":"10.1016/j.lfs.2025.124172","url":null,"abstract":"<div><h3>Aims</h3><div>Ovarian cancer (OV) is one of the most prevalent and life-threatening malignancies among women worldwide. Resistance to conventional therapies poses a major challenge in OV treatment. Ferroptosis, a type of programmed cell death driven by iron accumulation and marked by lipid peroxidation, has garnered significant attention in cancer research. The regulation of ferroptosis involves intricate epigenetic, transcriptional, and post-translational modification (PTM) processes. <em>O-</em>GlcNAcylation, a reversible PTM occurring on serine/threonine hydroxyl groups of proteins, has been connected with the regulation of apoptosis, autophagy, and necroptosis. However, its role in ferroptosis is still poorly understood.</div></div><div><h3>Materials and methods</h3><div><em>O</em>-GlcNAcylation levels and ferroptosis-associated markers were compared between normal and OV tissues. OV cells were subjected to ferroptosis induction using Erastin or RSL3, while <em>O</em>-GlcNAcylation was modulated via the OGT inhibitor OSMI-1 or the OGA inhibitor Thiamet-G. Subsequent analyses were performed to assess ferroptotic phenotypes and the c-MYC/xCT/GSH/GPX4 signaling pathway. In vitro findings were validated using a nude mouse xenograft model.</div></div><div><h3>Key findings</h3><div>In this study, we observed elevated <em>O</em>-GlcNAcylation, higher protein levels of xCT, GPX4, and FTH1, as well as increased antioxidant capacity in ovarian cancer tissues compared with normal ovarian tissues. Modulating <em>O</em>-GlcNAcylation levels in OV cells revealed that its downregulation enhanced ferroptosis, whereas upregulation inhibited it. Further investigation revealed that c-MYC protein levels were regulated by <em>O</em>-GlcNAcylation. The <em>O</em>-GlcNAcylation-mediated stabilization of c-MYC led to increased xCT expression, thereby enhancing the xCT/GSH/GPX4 antioxidant axis and suppressing ferroptosis in OV.</div></div><div><h3>Significance</h3><div>Our research may provide intervention strategies for the treatment of OV.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"387 ","pages":"Article 124172"},"PeriodicalIF":5.1,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145850305","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":"RUVBL1-mediated mTORC1 activation drives tumour progression and immune evasion for oral squamous cell carcinoma","authors":"Xinpei Wang ,&nbsp;Zuxuan Zhao ,&nbsp;Fengyang Jing ,&nbsp;Bingzhi Wang ,&nbsp;Meng Wang ,&nbsp;Jianming Ying ,&nbsp;Tiejun Li","doi":"10.1016/j.lfs.2025.124171","DOIUrl":"10.1016/j.lfs.2025.124171","url":null,"abstract":"<div><h3>Background and aims</h3><div>Oral squamous cell carcinoma (OSCC) is a prevalent head and neck malignancy for which surgical resection remains the primary therapeutic approach. Although immunotherapy, particularly immune checkpoint blockade targeting PD-1/PD-L1, has been revolutionary, only a small number of patients with OSCC have clinically benefited from it. Therefore, elucidating the molecular mechanisms underlying OSCC progression and immune evasion is crucial. RuvB-like AAA ATPase 1 (RUVBL1) has been implicated in diverse biological processes and modulates tumour immunity. Little is known regarding the function of RUVBL1 and its mechanism of action in OSCC. In this study, we aimed to understand RUVBL1 regulation in OSCC tissues and how expression correlates with patient prognosis.</div></div><div><h3>Materials and methods</h3><div>We conducted bioinformatics analysis, functional assays <em>in vitro</em>, co-culture experiments, and murine xenograft models, along with validation in clinical samples. To investigate the underlying mechanism, transcriptome sequencing and biochemical as well as molecular analyses were utilized.</div></div><div><h3>Key findings</h3><div>RUVBL1 promotes tumour growth and regulates the tumour microenvironment by controlling PD-L1 expression by targeting the rapamycin kinase (mTOR) pathway, thereby impairing both the infiltration and effector function of T cells in OSCC. Pharmacological inhibition of RUVBL1 with CB6644 suppressed tumour growth and synergised with PD-L1 blockade and conventional therapy. Collectively, these findings identify RUVBL1 as a critical driver of OSCC progression and immune modulation.</div></div><div><h3>Significance</h3><div>Our findings highlight the potential of RUVBL1 as a prognostic biomarker and therapeutic target to enhance treatment efficacy.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"386 ","pages":"Article 124171"},"PeriodicalIF":5.1,"publicationDate":"2025-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145846568","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":"FOSL2+ macrophages drive pro-inflammatory phenotype via miR-92a-3p/FOSL2/NF-κB axis to mediate endothelial cell injury in aortic dissection","authors":"Zhenpeng Yuan ,&nbsp;Ruihan Chen ,&nbsp;Rong Fan ,&nbsp;Zhenyu Yang ,&nbsp;Qianqian Zhu ,&nbsp;Chenyang Qiu ,&nbsp;Ziheng Wu ,&nbsp;Donglin Li ,&nbsp;Yangyan He ,&nbsp;Hongkun Zhang","doi":"10.1016/j.lfs.2025.124174","DOIUrl":"10.1016/j.lfs.2025.124174","url":null,"abstract":"<div><h3>Background</h3><div>In aortic dissection, macrophages play a critical role; however, the impact of macrophages on vascular endothelial cells remains unclear.</div></div><div><h3>Methods</h3><div>By constructing macrophage cell lines with stable overexpression and knockdown of FOSL2, M1 polarization was induced to evaluate the effects of FOSL2 on macrophage polarization, pro-inflammatory cytokine expression, macrophage migration, apoptosis, reactive oxygen species (ROS) generation, and mitochondrial function. Additionally, co-culture experiments were conducted to study the effects of macrophages with FOSL2 overexpression and knockdown on the proliferation, migration, apoptosis, and signaling pathways of mouse aortic endothelial cells (MAECs). Furthermore, miRNA prediction and validation experiments were performed to explore the regulatory mechanism of miR-92a-3p on FOSL2 and its role in macrophage-endothelial cell interactions.</div></div><div><h3>Results</h3><div>Overexpression of FOSL2 enhanced the expression and secretion of pro-inflammatory cytokines, promoting the M1 phenotype. It also increased macrophage migration, apoptosis, and ROS generation while suppressing mitochondrial membrane potential and activating the MYD88/TLR4/NF-κB signaling pathway. In co-culture experiments, FOSL2 overexpression in macrophages inhibited the proliferation and migration of co-cultured MAECs, promoted apoptosis and mitochondrial dysfunction, and upregulated endothelial injury markers and the PI3K/AKT/NF-κB signaling pathway. miR-92a-3p was downregulated during M1 polarization and directly targeted FOSL2, inhibiting its expression. Overexpression of miR-92a-3p reversed the FOSL2-mediated M1 polarization of macrophages and the functional impairment of co-cultured endothelial cells.</div></div><div><h3>Conclusion</h3><div>FOSL2 promotes macrophage M1 polarization by regulating the MYD88/TLR4/NF-κB signaling pathway, enhancing pro-inflammatory responses, and inhibiting the function of co-cultured endothelial cells. miR-92a-3p exerts the opposite effect by targeting FOSL2, suppressing M1 polarization and endothelial cell injury.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"388 ","pages":"Article 124174"},"PeriodicalIF":5.1,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145844040","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":"Temporal control of decidual inflammation by HOXA10 is essential for implantation and its dysregulation is associated with early pregnancy loss","authors":"R. Sharma ,&nbsp;B. Negi ,&nbsp;R. Ponsankaran ,&nbsp;S. Patil ,&nbsp;G. Godbole ,&nbsp;A. Mishra ,&nbsp;S. Shyamal ,&nbsp;D. Modi","doi":"10.1016/j.lfs.2025.124159","DOIUrl":"10.1016/j.lfs.2025.124159","url":null,"abstract":"<div><h3>Background</h3><div>Successful implantation requires tightly regulated endometrial inflammation. While initial inflammatory signaling is essential for implantation, persistent inflammation is detrimental to placentation and pregnancy maintenance. The molecular mechanisms that govern this temporal regulation remain unclear.</div></div><div><h3>Objective</h3><div>To investigate how the transcription factor HOXA10 modulates inflammatory transitions in decidual stromal cells and how its dysregulation contributes to implantation failure and early pregnancy loss.</div></div><div><h3>Methods</h3><div>We combined <em>in vitro</em> decidualization of primary human stromal cells with HOXA10 knockdown, transcriptomics, cytokine profiling, and adhesion assays. In parallel, inflammation and fertility were evaluated in <em>Hoxa10</em> hypomorphic mice. We re-analyzed publicly available bulk and single-cell RNA-seq (scRNA-seq) datasets from human endometrium and first-trimester decidua, focusing on inflammatory decidual stromal cell states to assess the clinical relevance of HOXA10 dysregulation in recurrent pregnancy loss (RPL).</div></div><div><h3>Results</h3><div>In mice, HOXA10 expression was transiently reduced at implantation but increased post-implantation. Transcriptome profiling revealed that <em>HOXA10</em> knockdown in decidualized stromal cells induced a pro-inflammatory phenotype along with altered expression of adhesion-related genes and impaired stromal–substrate adhesion. In non-pregnant <em>Hoxa10</em> hypomorphs, stromal cells showed elevated IL1β and TXNIP expression and activation of the NLRP3–ASC inflammasome, as well as dysregulated receptivity markers. During pregnancy, persistent HOXA10 deficiency prevented resolution of inflammation, leading to abnormal decidual organization and defective placentation. The hypomorphs had infertility or progressive reproductive decline. scRNA-seq of first-trimester human decidua showed that <em>HOXA10</em> is selectively low in inflammatory decidual stromal cell clusters that exhibit concordant upregulation of <em>IL1B, PYCARD, TXNIP</em>, and inflammasome components. Consistently, in bulk and single-cell datasets from women with recurrent pregnancy loss (RPL), <em>HOXA10</em> expression was reduced alongside increased inflammatory gene expression.</div></div><div><h3>Conclusions</h3><div>HOXA10 acts as a temporal switch that initiates inflammatory activation at implantation but is subsequently required to suppress inflammation, maintain stromal cell adhesion and organization, and support placentation. Loss of this regulatory switch results in persistent decidual inflammation and is associated with pregnancy loss in both mouse models and humans. The preprint version of this article is available at <span><span>https://doi.org/10.64898/2025.12.02.691844</span><svg><path></path></svg></span>.</div></div>","PeriodicalId":18122,"journal":{"name":"Life sciences","volume":"386 ","pages":"Article 124159"},"PeriodicalIF":5.1,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145844109","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}