Journal of Steroid Biochemistry and Molecular Biology最新文献

{"title":"Flavonoids as Promising Natural Therapeutics in Ovarian Cancer Treatment: A Comprehensive Review.","authors":"Yuan Chen, Xiaohua Tang, Yurong Zou, Dongwei Zhu, Selvaraj Muthusamy, Mangirish Deshpande, Natarajan Kiruthiga, Panneerselvam Theivendren, Kanagaran Rajalakshmi, Siyi Wu, Yisun Fan","doi":"10.1016/j.jsbmb.2026.107116","DOIUrl":"https://doi.org/10.1016/j.jsbmb.2026.107116","url":null,"abstract":"<p><p>Ovarian cancer (OC) remains one of the most lethal malignancies among women due to late-stage diagnosis and limited therapeutic options. The discovery of novel, effective treatments is crucial to improving patient outcomes. Flavonoids, a diverse group of polyphenolic compounds found abundantly in fruits, vegetables, and medicinal plants, have garnered significant attention for their anticancer properties, including their potential role in ovarian cancer treatment. This comprehensive review explores the molecular mechanisms underlying the anticancer effects of flavonoids in OC, highlighting their ability to modulate key signaling pathways involved in cell proliferation, apoptosis, invasion, and metastasis. Flavonoids exert their effects through antioxidant activity, inhibition of angiogenesis, and regulation of tumor suppressor genes and growth factors. Additionally, they interact with cellular signaling molecules such as the PI3K/Akt/mTOR, MAPK, and NF-κB pathways, influencing cell survival and death. Notably, flavonoids also enhance the cytotoxicity of chemotherapeutic agents, making them valuable adjuncts in OC therapy. This review further discusses the pharmacokinetics, bioavailability, and potential challenges in the clinical application of flavonoids as therapeutic agents for ovarian cancer. The findings suggest that flavonoids, due to their multifaceted mechanisms of action and relatively low toxicity, hold promise as adjunct or alternative therapies in the treatment of ovarian cancer. Future clinical trials are essential to validate their efficacy and safety in human OC patients.</p>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":" ","pages":"107116"},"PeriodicalIF":3.1,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to \"Molecular profile of androgen-independent prostate cancer xenograft LuCaP 23.1\" [J. Steroid Biochem. Mol. Biol. 96 (2005) 355-365].","authors":"F Fina, X Muracciole, P Rocchi, I Nanni-Métellus, C Delfino, L Daniel, C Dussert, L 'h Ouafik, P M Martin","doi":"10.1016/j.jsbmb.2026.107091","DOIUrl":"https://doi.org/10.1016/j.jsbmb.2026.107091","url":null,"abstract":"","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":" ","pages":"107091"},"PeriodicalIF":3.1,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endocrine disrupting effects of estrone on male Siniperca chuatsi: From gonadal remodeling to gene regulation.","authors":"Kaichun Chen, Yongqing Zhang, Weibin Li, Haiying Yang, Ziyan Deng, Guojun Cai, Zihang Xie, Qiang Li, Chong Han","doi":"10.1016/j.jsbmb.2026.107107","DOIUrl":"10.1016/j.jsbmb.2026.107107","url":null,"abstract":"<p><p>Estrone (E1), a ubiquitous environmental estrogen, poses a potential threat to the reproductive health of aquatic organisms. To evaluate the inducing effect of E1 exposure on gonadal feminization in male Siniperca chuatsi, male fish were exposed to 0, 0.01, 0.1, and 1 μg/L E1 for 60 days. The effects of E1 exposure on serum sex hormones, gonadal histological sections, vasa in situ hybridization, cell apoptosis, and gene expression in S. chuatsi were systematically examined. The results showed that 0.1 μg/L E1 treatment significantly inhibited testicular germ cell development, while 1 μg/L E1 treatment induced gonad histological feminization in 80% of male fish, with early vitellogenic oocytes appeared. Additionally, E1 exposure caused significant changes in serum sex hormones: 11-ketotestosterone levels significantly decreased, while immunoreactive estradiol levels significantly increased. Vasa gene in situ hybridization showed positive signals and TUNEL cell apoptosis revealed no obvious apoptotic signals in E1-induced histologically feminized gonads. Further molecular analysis revealed that sex regulation and development-related genes were involved in the E1-mediated gonadal feminization process: the expression of key male sex determination genes (dmrt1, amh, gsdf, sox9) and steroidogenic support genes (star, fshr) was significantly down-regulated, while expression of key female differentiation genes (bmp15, foxl2, cyp19a1a, hsd17b1) and germ cell development genes (sox19a, dazl, vasa, ccne2, sox3) was significantly up-regulated. Collectively, these findings demonstrate that E1 exposure induces histological testicular feminization in male S. chuatsi in a dose-dependent manner, concomitant with transcriptional downregulation of male differentiation genes and upregulation of female differentiation genes.</p>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":" ","pages":"107107"},"PeriodicalIF":3.1,"publicationDate":"2026-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148851584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pentadecanoic acid as a potential endogenous mTOR modulator for age-related female infertility: Mechanistic insights, molecular docking evidence, and therapeutic perspectives.","authors":"Reni Kalfin, Sidharth Mehan, Rajaram Samant, Manoj Tongra, Harsh Patil, Rohit Kumar Singh","doi":"10.1016/j.jsbmb.2026.107100","DOIUrl":"10.1016/j.jsbmb.2026.107100","url":null,"abstract":"<p><p>Age-related female infertility is a major reproductive health challenge that accelerates sharply after the age of 34, primarily due to declining oocyte quality, increased chromosomal abnormalities, and impaired embryonic developmental competence. Emerging evidence identifies chronic hyperactivation of the mechanistic target of rapamycin (mTOR) signalling pathway as a central molecular driver of ovarian aging, promoting excessive ribosome biogenesis, impaired proteostasis, suppressed autophagy, mitochondrial dysfunction, and oxidative stress within oocytes and surrounding cumulus cells. Although rapamycin, the prototypical mTOR inhibitor, has demonstrated promising effects in improving ovarian function and in vitro fertilization outcomes, its teratogenic potential, immunosuppressive properties, metabolic side effects, and prolonged pre-conception washout requirements limit its clinical applicability in fertility management. This review synthesises current evidence on the role of mTOR in ovarian aging and is complemented by an original molecular docking analysis performed by the authors to evaluate the interaction between pentadecanoic acid and the mTOR kinase domain, an endogenous odd-chain saturated fatty acid, as a potential fertility-safe mTOR modulator. A comprehensive review of the literature was conducted using PubMed and related databases, encompassing pentadecanoic acid biochemistry, molecular mechanisms, mTOR signalling architecture, ovarian aging biology, rapamycin pharmacology, and molecular docking studies. Available evidence indicates that pentadecanoic acid activates AMP-activated protein kinase (AMPK), modulates PPAR-α/δ signalling, supports cellular antioxidant defence, and collectively attenuates anabolic mTOR activity while promoting autophagic recycling and metabolic homeostasis. Molecular docking analysis against the mTOR kinase domain (PDB ID: 4JSV) demonstrated that pentadecanoic acid binds within the active site with a binding energy of -4.4 kcal/mol through interactions with key hydrophobic residues, including Leu1936, Ile1939, Tyr2144, Val2227, and Gly2142, whereas rapamycin exhibited a stronger affinity (-10.1 kcal/mol). Unlike rapamycin, pentadecanoic acid is endogenously produced, compatible with pregnancy, and requires no washout period. Collectively, these findings position pentadecanoic acid as a promising endogenous mTOR modulator with potential therapeutic relevance for age-related female infertility, warranting further mechanistic investigations and well-designed human clinical trials.</p>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":" ","pages":"107100"},"PeriodicalIF":3.1,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148714283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Targeting cholinesterases with steroid hormone derivatives: Insights from In Vitro assays and molecular modeling\" [J. Steroid Biochem. Mol. Biol. 258 (2026) 106950].","authors":"Jovana J Ajduković, Ana Matošević, Anita Bosak, Strahinja Kovačević, Milica Karadžić Banjac, Ivana Z Kuzminac, Andrea R Nikolić, Marina P Savić","doi":"10.1016/j.jsbmb.2026.107099","DOIUrl":"https://doi.org/10.1016/j.jsbmb.2026.107099","url":null,"abstract":"","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":" ","pages":"107099"},"PeriodicalIF":3.1,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148714334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the putative role of EGFR in prostate cancer: Interactions with androgen and estrogen receptors.","authors":"G M Gonçalves, D S Souza, C R M Costa, M E G Oliveira, C S Porto, C M Vicente","doi":"10.1016/j.jsbmb.2026.107101","DOIUrl":"10.1016/j.jsbmb.2026.107101","url":null,"abstract":"<p><p>The epidermal growth factor receptor (EGFR) is a transmembrane tyrosine kinase receptor that plays a critical role in regulating cell proliferation, survival, and differentiation. Aberrant activation or overexpression of EGFR has been observed in several cancers, including prostate cancer (PCa), and is associated with aggressive tumor behavior and poor prognosis. The development and progression of PCa largely depend on the involvement of androgen receptor (AR) pathways, which are directly related to EGFR signaling. Research indicates that EGFR can affect AR activity, increasing transcriptional activity or promoting ligand-independent activation, which may lead to castration-resistant prostate cancer (CRPC). Furthermore, emerging evidence suggests that estrogen receptors (ERs) may also interact with EGFR signaling in prostate tissue. These may influence tumor growth, interactions with cellular plasticity, and therapy resistance, but their exact mechanisms require further investigation. Identifying and improving treatment strategies for advanced and treatment-resistant PCa requires understanding the interplay between the EGFR, AR, and ER pathways. However, clinical trials have shown limited success in targeting EGFR alone, possibly through compensatory mechanisms via steroid hormone receptors. Therefore, therapies that simultaneously target EGFR and AR/ER activity may be more effective. Continued research into the molecular interplay between these pathways will broaden our understanding of prostate cancer biology and support the development of more personalized and effective treatments. In this review will focus on EGFR/HER1 and its putative role in prostate cancer. Furthermore, we discuss the potential interaction between EGFR, androgen receptor (AR), and estrogen receptor (ER) signaling pathways.</p>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":" ","pages":"107101"},"PeriodicalIF":3.1,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148708523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tissue-predominant estrogen metabolic remodeling in adenomyosis revealed by LC-MS/MS profiling.","authors":"Qing Wang, BoYang Liu, Lei Kuang, Lingke Wang, Yingying Chou, Bei Zhang, Guiping Wan, Tao Gui","doi":"10.1016/j.jsbmb.2026.107095","DOIUrl":"10.1016/j.jsbmb.2026.107095","url":null,"abstract":"<p><p>Adenomyosis (AM) is an estrogen-dependent gynecological disorder in which local steroid handling may contribute to clinical heterogeneity. To characterize estrogen metabolic features in AM, we used liquid chromatography-tandem mass spectrometry (LC-MS/MS) to quantify 13 estrogens and estrogen metabolites in endometrial tissue and serum. Tissue metabolite profiles showed marked increases in catechol estrogens, particularly 2-hydroxyestrone (2-OHE1) and 4-hydroxyestrone (4-OHE1), whereas serum changes were more limited, with 2-methoxyestrone (2-MeOE1) representing the main circulating difference. Pathway- and ratio-based analyses indicated enhanced hydroxylation in tissue without a proportionate increase in downstream methylation-related readouts. Correlation and regression analyses further showed that tissue 2-OHE1 and 4-OHE1 were independently associated with dysmenorrhea severity. In exploratory receiver operating characteristic analyses performed within the discovery cohort, tissue catechol estrogens showed stronger discriminatory ability than serum metabolites. These findings suggested that AM was associated with endometrial tissue-predominant remodeling of estrogen metabolism rather than with generalized elevation of parent estrogens. The present study identified candidate metabolic markers requiring further validation and provided a framework for future investigation of local steroid metabolism in AM.</p>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":" ","pages":"107095"},"PeriodicalIF":3.1,"publicationDate":"2026-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148631999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bis(monoacylglycero)phosphate protects murine RAW 264.7 macrophages against 7-Ketocholesterol-induced apoptosis and impaired autophagy","authors":"Remi Lambert ,&nbsp;Sherine Montillet ,&nbsp;Clara Hennot ,&nbsp;Agathe Diaz-Gonzalez ,&nbsp;Marion Guichard ,&nbsp;Emeline Cros-Perrial ,&nbsp;Lars Petter Jordheim ,&nbsp;Karen Gaget ,&nbsp;Federica Calevro ,&nbsp;Celine Luquain-Costaz ,&nbsp;Isabelle Delton","doi":"10.1016/j.jsbmb.2026.106955","DOIUrl":"10.1016/j.jsbmb.2026.106955","url":null,"abstract":"<div><div>Atherosclerosis, a leading cause of cardiovascular disease, is driven by the accumulation of oxidized low-density lipoproteins (oxLDL) in arterial walls. 7-Ketocholesterol (7KC), a major oxysterol found in oxLDL and atherosclerotic plaques, triggers multiple cell injuries including loss of lysosomal integrity, oxidative stress, apoptosis, and impaired autophagy in vascular cells. Bis(monoacylglycero)phosphate (BMP), also known as lysobisphosphatidic acid, is a unique phospholipid concentrated in the endolysosomal compartment, known to regulate vesicle dynamics, lysosomal enzyme activities, intracellular cholesterol trafficking and its oxidative metabolism. Using a validated model of BMP enrichment in murine RAW 264.7 macrophages, we investigated whether BMP could exert protective activity against 7KC-induced damage. Our findings revealed that BMP enrichment provides comprehensive protection against 7KC at the cellular level by preserving cell viability, morphology, and neutral lipid balance. Mechanistically, BMP enrichment prevented apoptosis by maintaining mitochondrial integrity and blocking caspase activation. This was demonstrated by normalized BAX/BCL2 ratios, preserved pro-Caspase-3 levels, and reduced PARP cleavage. Remarkably, BMP enrichment also restored autophagic flux, thereby preventing the pathological accumulation of LC3-II and p62 that characterizes autophagy dysfunction. Enhanced colocalization between LC3 and BMP suggests direct functional interactions in the stress response. Gene expression analysis confirmed that BMP enrichment normalized the transcriptional dysregulation of key autophagy regulators, including <em>Sqstm1</em>, <em>Becn1</em>, and <em>Pink1</em>. Taken together, these results suggest that BMP is an endogenous protective factor that counteracts 7KC-induced cellular damage at multiple steps by regulating cell death and autophagy pathways in a coordinated manner.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"259 ","pages":"Article 106955"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146182883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fenchone alleviates 7-ketocholesterol-induced oxiapoptophagy through activation of KLF4-PPARγ-Arg1-mediated M2 macrophage signalling","authors":"Sangeetha Ravi ,&nbsp;Livya Catherene Martin ,&nbsp;Manikandan Kumaresan ,&nbsp;Jaya Suriya Mani ,&nbsp;Beulaja Manikandan ,&nbsp;Manikandan Ramar","doi":"10.1016/j.jsbmb.2026.106951","DOIUrl":"10.1016/j.jsbmb.2026.106951","url":null,"abstract":"<div><div>7-ketocholesterol (7KCh), a cytotoxic oxysterol enriched in atherosclerotic plaques, provokes macrophage dysfunction through oxiapoptophagy, a linked process of oxidative stress, apoptosis and autophagy culminating in pro-inflammatory M1 polarization. Targeting this process could mitigate oxysterol-driven vascular inflammation. In this study, murine IC-21 macrophages were induced with 7KCh and co-exposed to fenchone, a bicyclic monoterpene with known anti-inflammatory properties. Cellular oxidative stress, apoptosis and autophagy were assessed by spectrofluorometric and cytometric assays. Expression of key mediators (iNOS, COX2, HO1, Casp3, Bcl2, LC3B, PARP1, Arg1, KLF4 and PPARγ) was quantified by RT-qPCR and western blotting. Molecular docking was used to identify interactions of fenchone with KLF4 and PPARγ. The results showed that 7KCh significantly increased ROS and NO production, disrupted mitochondrial membrane potential and induced apoptosis and autophagy in macrophages. Fenchone co-treatment counteracted these effects, restoring redox balance and membrane integrity. Molecular analyses revealed downregulation of iNOS, COX2, Casp3 and PARP1, alongside upregulation of HO1, Arg1, KLF4 and PPARγ. Docking analysis confirmed strong binding of fenchone to KLF4 and PPARγ, suggesting transcriptional regulation of macrophage polarization via the KLF4-PPARγ-Arg1 axis. These findings suggest that fenchone mitigates 7KCh-induced oxiapoptophagy and reprograms macrophages toward an anti-inflammatory M2 phenotype through modulation of KLF4/PPARγ signalling, positioning fenchone as a potential immunomodulatory candidate for combating oxysterol-mediated vascular inflammation.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"259 ","pages":"Article 106951"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What can we learn from the history of steroid metabolites and the ongoing identification of novel biologically active steroid metabolites?","authors":"Alex Odermatt ,&nbsp;David J. Morris","doi":"10.1016/j.jsbmb.2026.106954","DOIUrl":"10.1016/j.jsbmb.2026.106954","url":null,"abstract":"<div><div>Historically, it was thought that primary steroids released from endocrine glands exert their hormonal effects through corresponding receptors in peripheral tissues, and that their metabolism then inactivates them, followed by excretion. However, the metabolism of primary steroids is not just a way of inactivating and excreting them, but generates a variety of metabolites with different biological properties. In this review, we outline how various active steroid metabolites were discovered, describe some of the ways they are generated, and how they can in a non-classical way act on receptors or alter the activity of steroid metabolizing enzymes, thereby indirectly affecting receptor activities. Examples include the 5α-reduced ring-A metabolites of 11-deoxycorticosterone (DOC) and progesterone that are formed in the brain, act as neurosteroids and exert effects through the GABA-A membrane receptor. Another example is 11-ketoprogesterone that potently activates mineralocorticoid receptors (MR), but not glucocorticoid receptors (GR), and is more potent than its 11β-hydroxylated form, in contrast to glucocorticoids. Moreover, we discuss the microbiome as important source of bioactive metabolites, exemplified by the 11β-hydroxylated 5α-reduced ring-A corticosteroid and progesterone metabolites that were shown as potent 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) inhibitors. 11β-HSD2 inhibition results in cortisol-induced MR activation, sodium retention and hypertension. Furthermore, microbial 17,20-desmolase activity can convert glucocorticoids to androgens, potentially influencing diseases and therapeutic outcomes. There are still many knowledge gaps regarding bioactive steroid metabolites. Identifying additional bioactive steroid metabolites and characterizing their genomic and non-genomic effects should help uncovering their cell-specific functions and contributions to the maintenance of homeostatic regulation.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"259 ","pages":"Article 106954"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146182826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}