Journal of Steroid Biochemistry and Molecular Biology最新文献

{"title":"7-ketocholesterol as a critical oxysterol: Impact on human health and safety in food systems","authors":"Sheethal S Kumar,&nbsp;Akash Prakash,&nbsp;P.V. Keerthana,&nbsp;Mathew John","doi":"10.1016/j.jsbmb.2025.106856","DOIUrl":"10.1016/j.jsbmb.2025.106856","url":null,"abstract":"<div><div>7-Ketocholesterol (7-KC) is a biologically active oxysterol formed through the oxidation of cholesterol, predominantly under conditions of oxidative stress. It is generated both enzymatically in specific tissues such as the brain and liver, and non-enzymatically <em>via</em> reactive oxygen species (ROS), especially in aging tissues and heat-processed animal-derived foods. 7-KC exerts multifaceted effects on human health, extending beyond lipid metabolism to disrupt glucose and amino acid utilization, impair mitochondrial function, and provoke endoplasmic reticulum (ER) stress. These disturbances contribute to chronic inflammation and oxidative damage, playing pivotal roles in the development of various diseases, including atherosclerosis, neurodegenerative disorders, diabetes, cancer, hepatic steatosis, and ocular and gastrointestinal pathologies. Additionally, 7-KC is a marker of cholesterol oxidation in the food industry, where it signals product degradation and potential toxicity in long-stored or thermally processed animal-based foods. This review explores the biosynthesis, metabolic fate, and pathophysiological role of 7-KC, highlighting its critical role in intermediary metabolism, disease progression, and food safety. Furthermore, it outlines mitigation strategies to reduce 7-KC exposure through dietary modifications, antioxidant interventions, and advanced food processing technologies aimed at enhancing public health.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"255 ","pages":"Article 106856"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145016543","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":"Advancements in understanding the role and mechanisms of mitochondria in diabetes: A comprehensive review","authors":"Xia Ge ,&nbsp;Min Ye ,&nbsp;Aihua Fei ,&nbsp;Qingping Zhang ,&nbsp;Aihong Yuan","doi":"10.1016/j.jsbmb.2025.106875","DOIUrl":"10.1016/j.jsbmb.2025.106875","url":null,"abstract":"<div><div>Diabetes mellitus is a global health crisis with a rising prevalence attributed to complex interactions of genetic, lifestyle, and environmental factors. This comprehensive review delves into the pivotal role of mitochondrial dysfunction in the onset and progression of diabetes. It outlines how defects in mitochondrial oxidative phosphorylation, increased free radical production, and mitochondrial DNA damage contribute to insulin resistance, β-cell apoptosis, and systemic metabolic dysfunctions. The review highlights the critical roles of mitochondria in energy metabolism, oxidative balance, and the interplay of genetic and environmental factors in diabetes. It also emphasizes the association of impaired mitochondrial function with various diabetes-related complications and organ-specific diseases, underscoring the urgent need for innovative therapeutic strategies. Potential interventions discussed include pharmacological agents promoting mitochondrial biogenesis and enhancing mitochondrial dynamics, alongside dietary and lifestyle modifications that support mitochondrial function and overall metabolic health. The review calls for intensified research into mitochondrial mechanisms and their therapeutic targets, advocating for comprehensive clinical trials and support from medical and governmental institutions to advance diabetes management strategies centered on mitochondrial health.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"255 ","pages":"Article 106875"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253504","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":"Zingerone supplementation affects proliferation, apoptosis, antioxidant, GLUT4 and insulin receptor expression in uterus of mice","authors":"Ayushmita Dutta,&nbsp;Guruswami Gurusubramanian,&nbsp;Vikas Kumar Roy","doi":"10.1016/j.jsbmb.2025.106885","DOIUrl":"10.1016/j.jsbmb.2025.106885","url":null,"abstract":"<div><div>Zingerone has various biological properties with a modulatory role in ovarian activity. Despite its biological property, its effect has not been investigated on the uterus. Therefore, the present study has investigated the effects of zingerone supplementation on uterus of mice. Female Swiss albino mice were randomly divided into four groups: control, Z10, Z25, and Z50, where zingerone was orally given for 28 days. Zingerone treatment at 25 and 50 mg/kg increased the number of uterine glands. Immunolocalization of PCNA was decreased in the in vivo study, while in vitro BrdU incorporation was stimulated by the zingerone. Zingerone treatment increased apoptosis at a 25 mg/kg dose; however, zingerone at a 50 mg/kg dose decreased uterine apoptosis. In vitro study also showed zingerone down-regulates BCL2 expression and up-regulates active caspase expression. These findings suggest modulatory effects of zingerone on uterine proliferation and apoptosis. The pro-inflammatory TNFα showed the lowest expression in 50 mg/kg zingerone-treated mice uterus. In vitro findings also showed that zingerone decreased expression of TNFα. Furthermore, an in vivo study has also shown zingerone down-regulates INSR and GLUT4 without affecting uterine glucose concentration. In addition, an in vitro study has also shown that zingerone down-regulates INSR. Zingerone treatment showed elevated MDA levels and GPX enzyme activity. However, SOD activity was suppressed in 25 and 50 mg/kg groups. Furthermore, catalase activity was highest in the 50 mg/kg zingerone-treated group. Thus, these results showed the modulatory role of zingerone on apoptosis, glucose metabolism, and antioxidant status in uterus. The functional significance of zingerone-mediated parameters on uterine functions remains to be investigated.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"255 ","pages":"Article 106885"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145426906","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":"Why 7-ketocholesterol matters now: A rapid review of its pathogenic and therapeutic relevance","authors":"Evelyn Sharon Sukumaran ,&nbsp;Arin Natania S","doi":"10.1016/j.jsbmb.2025.106865","DOIUrl":"10.1016/j.jsbmb.2025.106865","url":null,"abstract":"<div><div>7-Ketocholesterol (7-KC), a major oxysterol formed through cholesterol autoxidation, is increasingly recognized as a pathogenic mediator in ageing and chronic disease. Detected in atherosclerotic plaques, Alzheimer’s cortex, aged retina, and lysosomal storage disorders, 7-KC actively drives oxidative stress, chronic inflammation, organelle dysfunction, and oxiapoptophagy. These mechanisms underpin its role in cardiovascular, neurodegenerative, and metabolic pathologies. Recent advances highlight nutritional antioxidants, pharmacological agents, microbial bioremediation, and nanotechnology as promising therapeutic avenues. Recognizing 7-KC as both a biomarker and therapeutic target offers opportunities for innovation in diagnostics and treatment of age-related and inflammatory disorders.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"255 ","pages":"Article 106865"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145097892","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":"Indole-3-propionic acid function through PXR and AhR, molecular signaling pathways, and antitoxic role in underlying diseases","authors":"Cyrus Jalili ,&nbsp;Foruzan Hosseinkhani ,&nbsp;Dian Dayer ,&nbsp;Mohammad Reza Tabandeh ,&nbsp;Ardeshir Abbasi ,&nbsp;Touraj Zamir Nasta","doi":"10.1016/j.jsbmb.2025.106877","DOIUrl":"10.1016/j.jsbmb.2025.106877","url":null,"abstract":"<div><div>The host organism's balance within the body relies on its crucial symbiotic relationship with gut microbiota. This balance, known as homeostasis, can be influenced by various factors. One significant factor is the role of bacterial metabolites from different substrates, such as tryptophan. Recent research has revealed that these metabolites impact many biological processes. Microbial metabolites, such as Indole-3-Propionic Acid (IPA), are produced by the intestinal microbiota by converting dietary tryptophan. IPA is absorbed by intestinal epithelial cells, transported via the portal circulation, undergoes minimal hepatic metabolism, and is subsequently released into the systemic circulation to reach peripheral tissues and exert its biological effects. The Pregnane X receptor (PXR) and aryl hydrocarbon receptor (AhR) are the two main receptors of IPA which induce different gene expression profiles and subsequently diverse biological pathways in different tissues. Once absorbed by intestinal epithelial cells, IPA is released into the circulatory system and can significantly affect the immune, cardiovascular, nervous, and gastrointestinal systems. Furthermore, IPA has been found to have positive effects on a cellular level by inhibiting oxidative stress injury and preventing the synthesis of proinflammatory cytokines. Numerous studies have highlighted IPA's antioxidant, anti-inflammatory, anti-cancer, and neuroprotective effects. Therefore, dysbiosis of IPA contributes to disorders such as metabolic syndromes, inflammatory conditions, cancer, and neuropsychiatric diseases. This review provides a detailed examination of the most recent studies on indole-3-propionic acid function through PXR and AhR, outlining its molecular signaling pathways and correlation with various diseases.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"255 ","pages":"Article 106877"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145304358","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":"Network pharmacology-guided systems biology reveals β-Sitosterol’s multi-target role in reversing 7-ketocholesterol-induced oxidative and inflammatory stress","authors":"Nila Ganamurali ,&nbsp;Sarvesh Sabarathinam","doi":"10.1016/j.jsbmb.2025.106863","DOIUrl":"10.1016/j.jsbmb.2025.106863","url":null,"abstract":"<div><div>7-Ketocholesterol (7-KC), a cytotoxic oxysterol generated through cholesterol oxidation, plays a central role in the progression of atherosclerosis, neurodegeneration, and metabolic syndromes through mitochondrial dysfunction, ROS overproduction, and NLRP3 inflammasome activation. This study presents the first integrative systems pharmacology analysis exploring the molecular mechanisms by which β-sitosterol (BS), a phytosterol with antioxidant and anti-inflammatory properties, mitigates 7KC-induced toxicity. Shared targets between BS and 7KC were identified through target prediction databases and subjected to protein–protein interaction (PPI) network analysis using Cytoscape with bottleneck centrality. Top hub genes were functionally enriched using Gene Ontology and KEGG pathway tools, revealing BS’s modulation of nuclear receptor activity, redox homeostasis, and OXPHOS pathways. BS targets were localized across cytosol, nucleus, and membrane compartments, supporting its multi-compartmental regulatory role. This mechanistic framework highlights BS as a potential nutraceutical intervention for 7KC-driven chronic diseases, including atherosclerosis, NAFLD, and Alzheimer’s disease, warranting further biological validation.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"255 ","pages":"Article 106863"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145050223","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":"Vitamin D pathway as a multi-level predictor of COVID-19 severity and mortality: Integrating serum levels, FokI (rs2228570) VDR polymorphism, and lung tissue expression","authors":"Harem Khdir Awla ,&nbsp;Baghawan Ahmed Othman ,&nbsp;Dawan dlshad rafeeq ,&nbsp;Shukur Wasman Smail ,&nbsp;Raya Kh. Yashooa ,&nbsp;Asmaa Ameen Ghareeb ,&nbsp;Rebaz Hamza Salih ,&nbsp;Shwan Ali Omar ,&nbsp;Christer Janson","doi":"10.1016/j.jsbmb.2025.106879","DOIUrl":"10.1016/j.jsbmb.2025.106879","url":null,"abstract":"<div><h3>Background</h3><div>Vitamin D is a known immunomodulator, but its predictive value in COVID-19 remains incompletely understood. This study investigates the role of vitamin D across molecular, biochemical, and histopathological levels to evaluate its association with COVID-19 severity and mortality.</div></div><div><h3>Methods</h3><div>A prospective case-control study was conducted in the Kurdistan Region of Iraq from May to October 2021. Ninety-five confirmed COVID-19 patients (75 survivors, 20 non-survivors) and 75 healthy controls were enrolled. Serum 25(OH)D levels were quantified by ELISA. Clinical severity was assessed using CURB-65, NEWS, and SOFA scores. Genotyping for the <em>Fok</em>I (rs2228570) polymorphism in the VDR gene was performed via allele-specific PCR. Lung tissue from five survivors (biopsy) and five non-survivors (autopsy) underwent immunohistochemical staining to evaluate VDR expression.</div></div><div><h3>Results</h3><div>Serum vitamin D concentrations were markedly reduced in non-survivors (20.34 ± 0.46 ng/mL) relative to survivors (40.11 ± 0.28 ng/mL, p &lt; 0.001). Vitamin D exhibited a negative correlation with CURB-65 (r = –0.828), NEWS (r = –0.794), and SOFA (r = –0.762) scores. Regression analysis established that vitamin D was independently associated with disease severity in our population. The TT genotype of the <em>Fok</em>I VDR polymorphism correlated with markedly reduced vitamin D levels and elevated severity scores. Mortality exhibited a strong association with the TT genotype (OR = 10.29, 95 % CI: 2.204–49.19, p = 0.003) and the T allele (OR = 3.923, p = 0.0006). ROC analysis determined a vitamin D threshold of ≤ 20.56 ng/mL as indicative of mortality (AUC = 0.784, p &lt; 0.0001). Immunohistochemistry demonstrated elevated VDR expression in lung tissues of deceased COVID-19 patients relative to VDR-negative controls.</div></div><div><h3>Conclusion</h3><div>This study indicates that serum vitamin D levels, VDR gene polymorphism (rs2228570), and lung tissue VDR expression are strongly correlated with the severity and mortality of COVID-19. These findings validate the clinical use of vitamin D and VDR profiling may have associative markers and prospective treatment targets in the management of COVID-19.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"255 ","pages":"Article 106879"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145362994","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":"The benefit of mineralocorticoid receptor blockade in the treatment of experimental autoimmune encephalomyelitis mice","authors":"Franco Veloso ,&nbsp;Sofía D'Alessandro ,&nbsp;Analia Lima ,&nbsp;Paulina Roig ,&nbsp;Alejandro F. De Nicola ,&nbsp;Laura I. Garay","doi":"10.1016/j.jsbmb.2025.106844","DOIUrl":"10.1016/j.jsbmb.2025.106844","url":null,"abstract":"<div><div>Research on the effects of the mineralocorticoid receptor (MR) suggested a role in innate and adaptive immune responses. The inflammatory profile is directly linked to MR activation in several pathologies such as cardiovascular diseases, autoimmunity, chronic renal disease and obesity. MR is a high-affinity receptor binding both mineralocorticoids and glucocorticoids. In this study, we explored the pharmacological modulation of MR with the mineralocorticoid agonist deoxycorticosterone (DOCA) and the antagonist spironolactone (SPIRO) on corticosterone levels in plasma, neuroinflammation, myelin status and neurodegeneration in the spinal cord of mice with experimental autoimmune encephalomyelitis (EAE) model of Multiple Sclerosis. Animals were treated from day 1 until sacrificed on day 17 post-induction, and experimental groups were divided into: EAE+DOCA (0.75 mg/kg s.c every 3 days), EAE+DOCA+SPIRO (Spironolactone: 25 mg/kg i.p daily), vehicle-treated EAE (EAE+VEH) and Control (CTRL). Administration of DOCA or vehicle to EAE conducted to similar neuropathological alterations. The MR antagonist (a) significantly decreased inflammatory parameters TLR4, IL-1β and microglial CD11b mRNAs and showed a tendency to reduced osteopontin, b) reduced the % of infiltrated cellular and demyelinated area, as well as the reactive gliosis (GFAP+ area and number of IBA1 + cells) vs EAE+DOCA (c) increased the area of the neuronal marker NeuN vs EAE+DOCA and EAE+VEH groups (d) improved functional performance in the rotarod test and clinical signs vs EAE+DOCA. Interestingly, plasma corticosterone was increased in EAE+VEH and EAE+DOCA vs CTRL, while SPIRO administration raised even more corticosterone levels. This hypercorticosteronemia had functional consequences, because the glucocorticoid receptor (GR) and the target gene serum glucocorticoid regulated kinase 1 (SGK1) mRNAs expression were also increased vs DOCA alone. We hypothesized that MR blockage with SPIRO downregulated inflammation-related spinal cord pathology whereas excess glucocorticoids circulating in the EAE+DOCA+SPIRO group may contribute to anti-inflammatory effects.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"254 ","pages":"Article 106844"},"PeriodicalIF":2.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144895522","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":"Nano-curcumin attenuates tamoxifen resistance and malignant progression in ER-positive breast cancer cells by inhibiting the PI3K/AKT/mTOR signaling pathway","authors":"Chenguang Zhang,&nbsp;Hu Wang,&nbsp;Hao Lei,&nbsp;Jianghua Ou","doi":"10.1016/j.jsbmb.2025.106825","DOIUrl":"10.1016/j.jsbmb.2025.106825","url":null,"abstract":"<div><div>Breast cancer (BC) is one of the most prevalent malignant tumors among women, with estrogen receptor (ER)-positive patients constituting approximately 70 % of all cases. Endocrine therapy is currently a treatment option for patients with ER-positive BC; however, the development of resistance significantly limits the effectiveness of this treatment. Nano-curcumin (Nano-CUR) possesses anticancer properties and enhances bioavailability by improving the hydrophobic character of curcumin (CUR). However, the underlying mechanism by which Nano-CUR affects tamoxifen (TAM) resistance in ER-positive BC remains unknown. Here, we found that Nano-CUR promoted apoptosis and cell cycle arrest, inhibited cell proliferation and reduced the levels of cancer stem cells (CSCs)-related markers, including octamer-binding protein (OCT4), Nanog homeobox (NANOG) and sex-determining region Y-box 2 (SOX2) in TAM-resistant BC cells. Additionally, Nano-CUR demonstrated the ability to inhibit tumor malignant progression in TAM-treated BC mice. Mechanistically, Nano-CUR blocked the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway in MCF-7/TAM and T47D/TAM cells. The activation of this pathway by its activators (PI3K activator 740Y-P, AKT activator SC-79, and mTOR activator MHY1485) effectively alleviated the anti-tumor effect induced by Nano-CUR in TAM-resistant BC cells. Collectively, these findings reveal that Nano-CUR contributes to the reduction of tumorigenesis and TAM resistance in ER-positive BC cells by inhibiting the PI3K/AKT/mTOR signaling pathway.</div></div>","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"254 ","pages":"Article 106825"},"PeriodicalIF":2.7,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144568068","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 “Analysis of star promoter in common carp and catfish testis: Role of c-jun and its association with testicular function as a transcription factor” [J. Steroid Biochem. Mol. Biol. 253 (2025) 106817]","authors":"Swathi Tenugu,&nbsp;Balasubramanian Senthilkumaran","doi":"10.1016/j.jsbmb.2025.106847","DOIUrl":"10.1016/j.jsbmb.2025.106847","url":null,"abstract":"","PeriodicalId":51106,"journal":{"name":"Journal of Steroid Biochemistry and Molecular Biology","volume":"254 ","pages":"Article 106847"},"PeriodicalIF":2.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145001894","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}