Molecular and Cellular Endocrinology最新文献

{"title":"Glial activation and increased blood brain barrier permeability in the medial preoptic area of male mice lacking neural androgen receptor","authors":"Nida Karameh ,&nbsp;Afnan Atallah ,&nbsp;Danaé Nuzzaci ,&nbsp;Valérie Grange-Messent ,&nbsp;Sakina Mhaouty-Kodja","doi":"10.1016/j.mce.2026.112742","DOIUrl":"10.1016/j.mce.2026.112742","url":null,"abstract":"<div><div>We have previously shown that testosterone depletion in adult male mice induced neural androgen receptor (<em>Ar</em>) down-regulation and led to neuroinflammation and increased blood brain barrier (BBB) permeability in the medial preoptic area. In the present study, we investigated the effects of neural <em>Ar</em> deletion on glial function and BBB integrity in male mice. For this purpose, we used control and mutant littermates obtained from a mouse line deleted for the <em>Ar</em> in neural progenitors by Cre-loxP technology. Neural <em>Ar</em> deletion induced glial activation evidenced by increased immunoreactivity against markers of astrocytes (glial fibrillary acidic protein -GFAP- and N-myc downstream-regulated gene 2) and microglia (ionized calcium binding adaptor molecule 1). Fluoro-Jade® C fluorescent labeling was increased and inflammatory molecules such as inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX2) were detected in the vicinity of capillaries in the male medial preoptic area of neural <em>Ar</em> knockout mice. Analysis of BBB integrity showed enhanced permeability for Evans Blue tracer and endogenous immunoglobulins in mutant animals compared to their control littermates. In addition, modifications in the ultrastructural organization of capillary endothelial tight junctions were observed by electron tomography. These effects were specific to neural <em>Ar</em> deletion since no changes were observed for GFAP-immunoreactivity, BBB permeability or Fluoro-Jade® C labeling in male mice expressing the wild type <em>Ar</em> allele and carrying the Cre transgene.</div><div>Altogether, these data indicate the key role of the neural AR in testosterone-induced regulation of astrocyte, microglial and BBB functions in the medial preoptic area of male mice.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"615 ","pages":"Article 112742"},"PeriodicalIF":3.6,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146049005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperglycemia differentially regulates osteoblast and osteoclast autophagy via AMPK/mTOR/p70 S6K signaling in diabetic osteoporosis","authors":"Bin Zhou ,&nbsp;Fen Feng ,&nbsp;Cila Zhou ,&nbsp;Kuang Yao ,&nbsp;Ping Huang","doi":"10.1016/j.mce.2026.112739","DOIUrl":"10.1016/j.mce.2026.112739","url":null,"abstract":"<div><div>Type 2 diabetes mellitus (T2DM) often induces diabetic osteoporosis (DOP) with impaired bone remodeling, yet its underlying mechanism remains elusive. This study identified the differential regulatory role of the AMPK/mTOR/p70 S6K signaling axis in bone cell function. In vivo, diabetes reduced AMPK phosphorylation, enhanced mTOR/p70 S6K activation, and diminished autophagy in rat femoral tissue. In vitro, HG exerted cell-type-specific effects via the AMPK signaling pathway: in osteoblasts, HG inhibited AMPK phosphorylation, activated mTOR/p70 S6K, suppressed autophagy, and impaired mineralization as well as alkaline phosphatase (ALP) activity; conversely, in osteoclasts, HG enhanced autophagy through the inverse regulatory pathway and accelerated osteoclast differentiation and bone resorption. Collectively, these findings illustrate that hyperglycemia disrupts bone homeostasis via cell-type-specific regulation of AMPK, suggesting that AMPK-mediated autophagy serves as a potential critical therapeutic target for diabetes-related bone diseases.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"615 ","pages":"Article 112739"},"PeriodicalIF":3.6,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146086432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The implementation of small molecule agonists and antagonists to elucidate gonadotropin receptor structure, function and physiology.","authors":"James A Dias, Claire L Newton, Alfredo Ulloa-Aguirre","doi":"10.1016/j.mce.2026.112735","DOIUrl":"10.1016/j.mce.2026.112735","url":null,"abstract":"<p><p>Pursuant to patient desires of alternatives to injectable gonadotropins, a plethora of attempts have identified, characterized, and demonstrated efficacy of small molecules that activate (agonists) gonadotropin receptors. Discoveries have also been made of small molecule gonadotropin receptor inhibitors (antagonists), which have potential as useful alternatives to steroid hormone-based contraception. Implementation of these small molecules in advanced testing systems not necessarily used in screening, which identified lead compounds, has yielded a bounty of wonders. It is likely that a richer understanding of the role of signaling platforms and conformation-dependent molecular assemblies are likely to emerge. Several small molecule agonists have been observed to function as conformational boosters that can rescue receptor trafficking defects, or initiate internalization of receptors without bound hormone. Still others have revealed insights into the role of molecular platforms in persistent signaling. Unexpectedly, such antagonists, like molecular scalpels, can ablate certain signaling pathways and not others leading to discovery of biased signaling in gonadotropin receptors. That seminal observation has led to studies of nuanced signaling and, consequently, nuanced gene expression. Gonadotropin receptor structure-based design for better specificity and potency of agonists and antagonists has been provided by new cryo-EM structures of the gonadotropin receptors, demonstrating proof of concept. Structural determination of downstream supramolecular assemblies will be necessary to validate and fully understand these complicated receptors and how their interaction with other proteins and when occupied by hormone and allosteric modulators, nuances their actions and, ultimately, fertility.</p>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":" ","pages":"112735"},"PeriodicalIF":3.6,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146030280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring recent insights on intermittent fasting in regulating glucocorticoid levels and diet-induced metabolic disorders with focus on MAFLD and hepatic outcomes","authors":"Jasper Okoro Godwin Elechi ,&nbsp;Carolina Ramos de Mendonça ,&nbsp;Vitor Carlos de Araújo Bandeira ,&nbsp;Maria Surama Pereira Da Silva ,&nbsp;Ana Paula Rocha de Melo ,&nbsp;Rubem Carlos Araujo Guedes ,&nbsp;Sandro Massao Hirabara ,&nbsp;Erika Cione ,&nbsp;Diogo Antonio Alves de Vasconcelos","doi":"10.1016/j.mce.2026.112736","DOIUrl":"10.1016/j.mce.2026.112736","url":null,"abstract":"<div><div>Consumers' risky eating behaviours aided by the current food environment have led to an increase in diet-related metabolic disorders. Metabolic (dysfunction)-associated fatty liver disease origin represents a major global health burden that is increasing at an alarming rate on an annual basis. Modifying the timing of calorie consumption, dietary composition, or caloric intake offers a promising therapeutic approach for the management of this condition. The aim of this review was to provide a concise analysis of the impact of intermittent fasting on the regulation of glucocorticoid levels and diet-induced metabolic disorders with a focus on non-alcoholic fatty liver diseases. We found that intermittent fasting primarily regulates hepatic autophagy via nutritional and hormonal pathways, aiding in the maintenance of energy equilibrium, enhancement of mitochondrial function, regulation of liver quality, preservation of cellular homeostasis, protection of cells from harmful factors, mitigation of liver metabolic disorders, and improvement of liver inflammation. Also, the physiological changes induced by intermittent fasting and their metabolic consequences arise through multiple mechanisms, including alterations in hepatic metabolism, hepatic autophagy, inflammatory responses, liver functional enzymes, hepatic steatosis, fibroblast growth factor signalling, White adipoe tissue browning, adipokines, circadian rhythms, lipid profiles, body composition, the adipose tissue–gut microbiome axis, skeletal muscle, and the autophagy process. Interestingly, we identified the complex interplay among glucocorticoids, intermittent fasting, and non-alcoholic fatty liver diseases highlighting the hepatic macrophage glucocorticoid receptor as a pivotal mediator of fasting-induced reprogramming of the macrophage secretome, including fasting-suppressed cytokines. In conclusion, existing data indicates that intermittent fasting in patients with non-alcoholic fatty liver diseases is a viable, safe, and successful strategy for weight reduction, demonstrating notable trends in the amelioration of dyslipidaemia and non-alcoholic fatty liver diseases.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"614 ","pages":"Article 112736"},"PeriodicalIF":3.6,"publicationDate":"2026-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146003723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “The local corticotropin-releasing hormone receptor 2 signalling pathway partly mediates hypoxia-induced increases in lipolysis via the cAMP–protein kinase A signalling pathway in white adipose tissue” [Mol. Cellul. Endocrinol. 392/1–2 (2014) 106–114]","authors":"Yanlei Xiong ,&nbsp;Zhuan Qu ,&nbsp;Nan Chen ,&nbsp;Hui Gong ,&nbsp;Mintao Song ,&nbsp;Xuequn Chen ,&nbsp;Jizeng Du ,&nbsp;Chengli Xu","doi":"10.1016/j.mce.2025.112680","DOIUrl":"10.1016/j.mce.2025.112680","url":null,"abstract":"","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"614 ","pages":"Article 112680"},"PeriodicalIF":3.6,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145998637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"circPTPRM can encode a functional polypeptide circPTPRM-187aa to promote papillary thyroid carcinoma progression","authors":"Chengzhou Lv,&nbsp;Jiapeng Huang,&nbsp;Xiaoyu Ji,&nbsp;Wei Sun,&nbsp;Hao Zhang","doi":"10.1016/j.mce.2026.112734","DOIUrl":"10.1016/j.mce.2026.112734","url":null,"abstract":"<div><h3>Aims</h3><div>Papillary thyroid carcinoma (PTC) is the most common thyroid tumor, usually with a good prognosis, though some cases show early invasion, metastasis, and may become iodine-refractory. circRNAs can interact with miRNAs, bind proteins, regulate transcription, and encode polypeptides, but their translation function in thyroid cancer remains unexplored.</div></div><div><h3>Methods</h3><div>Quantitative real-time PCR (qRT-PCR), agarose gel electrophoresis, circRNA stability assessment, fluorescence in situ hybridization (FISH) were performed to explore the expression profile of circPTPRM in PTC tissues and adjacent non-cancerous thyroid tissues. We performed molecular biological and cell function experiments by constructing knockdown and various overexpression vectors. Effects of circPTPRM on PTC tumorigenesis were investigated through in vitro and in vivo experiments. The mechanism of circPTPRM-mediated tumor promotion was explored through immunofluorescence (IF), LC-MS/MS, immunoprecipitation (IP) and Co-immunoprecipitation (Co-IP), protein stability assessment, and ubiquitination assay.</div></div><div><h3>Results</h3><div>We confirmed that circPTPRM influenced PTC cell proliferation, migration, invasion through its translated polypeptides. In vivo experiments with nude mouse tumors also demonstrated that overexpression of circPTPRM contributed to the tumor's increased volume and weight. Subsequently, in the mechanistic analysis we found that circPTPRM-187aa polypeptide could bind IQGAP1 and induce TGF-β pathway activation by elevating RAC1 and CDC42.</div></div><div><h3>Conclusion</h3><div>CircPTPRM can encode circPTPRM-187aa polypeptide. circPTPRM-187aa, regulates the expression of IQGAP1 protein, and up-regulates RAC1 and CDC42 proteins in TGF-β signaling pathway, enhancing the PTC cells proliferation, migration, and invasion.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"614 ","pages":"Article 112734"},"PeriodicalIF":3.6,"publicationDate":"2026-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hsp90α as a promising therapeutic target for suppressing tumor progression in Lactotroph PitNETs","authors":"Jie Wu,&nbsp;Zhengan Zhou,&nbsp;Chongxue Ding,&nbsp;Hongjie Sun,&nbsp;Ming Xia,&nbsp;Kai Zhou,&nbsp;Tingrong Zhang,&nbsp;Shaoshan Li","doi":"10.1016/j.mce.2026.112733","DOIUrl":"10.1016/j.mce.2026.112733","url":null,"abstract":"<div><h3>Background</h3><div>Aggressive Lactotroph Pituitary Neuroendocrine Tumors (Lactotroph PitNETs) usually exhibit invasive growth behavior and resistance to dopamine agonists, showing difficulty in radical treatment and a high recurrence rate. Heat shock protein 90α(Hsp90α),a pivotal isoform of the heat shock protein 90(Hsp90) family, acts as a central chaperone that stabilizes numerous oncoproteins driving tumor progression, but its role in Lactotroph PitNETs remains unclear.</div></div><div><h3>Objective</h3><div>To study the effect of Hsp90α knockdown on the proliferation and invasiveness of Lactotroph PitNETs cells (MMQ).</div></div><div><h3>Methods</h3><div>Hsp90α and EGFR expression was compared between 18 aggressive and 22 Non-Aggressive human Lactotroph PitNETs by IHC and immunofluorescence. MMQ rat lactosomatotroph cells were transduced with lentiviral shRNA targeting Hsp90α(shHsp90α). Cell proliferation (CCK8),apoptosis (Annexin-V/7-AAD flow cytometry), Prolactin (PRL) secretion (ELISA), migration and invasion (Transwell) were assessed. Western blotting evaluated EGFR,<strong>PRL</strong>,AKT,ERK1/2,mTOR,p-AKT,p-ERK1/2 and p-mTOR.</div></div><div><h3>Results</h3><div>Aggressive Lactotroph PitNETs displayed higher Hsp90α and EGFR expression and showed a notable degree of spatial overlap. Hsp90α knockdown reduced EGFR,AKT,ERK1/2,mTOR,p-AKT,p-ERK1/2 and p-mTOR levels, decreased proliferation, increased apoptosis, lowered PRL secretion, and impaired migration and invasion.</div></div><div><h3>Conclusions</h3><div>Hsp90α knockdown simultaneously destabilizes EGFR and its downstream AKT/mTOR and ERK axes, resulting in multi-modal suppression of Lactotroph PitNETs invasion. Targeting Hsp90α may offer a novel therapeutic strategy for Aggressive Lactotroph PitNETs refractory to standard medical therapy.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"614 ","pages":"Article 112733"},"PeriodicalIF":3.6,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145979822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental exposure to a mixture of propiconazole and glyphosate induces histopathological lesions in the prostate of postpubertal rats","authors":"Ayelen L. Gomez ,&nbsp;Débora G. Reato ,&nbsp;Eduardo Masat ,&nbsp;Laura Kass ,&nbsp;Gabriela A. Altamirano","doi":"10.1016/j.mce.2026.112730","DOIUrl":"10.1016/j.mce.2026.112730","url":null,"abstract":"<div><div>Pesticide mixture exposure during critical developmental windows is a growing public health concern, given their potential additive or synergistic effects on the male reproductive system. This study aimed to evaluate whether developmental exposure to a mixture of propiconazole (PRO) and glyphosate (GLY) alters the postpubertal rat prostate. Pregnant rats were orally exposed to vehicle (saline) or a mixture of PRO and GLY (4 mg PRO/kg/day and 3.7 mg GLY/kg/day) from gestation day 9 until weaning. On postnatal day 60, male offspring were euthanized, and the prostate and serum samples were collected. PROGLY-exposed rats exhibited changes in the ventral and dorsolateral prostate histoarchitecture, including epithelial and stromal remodeling and increased incidence of prostate lesions. In the ventral prostate, although the relative glandular area remained unchanged, PROGLY exposure exhibited increased epithelial height and decreased luminal acinar area. Also, hyperplastic and atrophic acini were more prevalent in these animals. PROGLY exposure reduced estrogen receptor beta (ESR2) protein level, particularly in hyperplastic and atrophic acini, without affecting androgen or estrogen receptor alpha. ESR2 decrease was associated with an increased cell proliferation index in hyperplastic acini and a reduction in serum testosterone level in PROGLY-exposed rats. Stromal alterations included increased smooth muscle cell layers and reduced vimentin-positive fibroblasts, with no evidence of myofibroblast presence. This study shows that developmental exposure to PROGLY disrupts normal ventral prostate architecture and hormone signaling in postpubertal rats. These findings highlight the potential long-term risks of combined pesticide exposure on male reproductive health and the importance of evaluating mixture effects.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"614 ","pages":"Article 112730"},"PeriodicalIF":3.6,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145908767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative advances in endocrine oncology: From unique glimpses to familiar themes","authors":"Shereen Ezzat","doi":"10.1016/j.mce.2025.112723","DOIUrl":"10.1016/j.mce.2025.112723","url":null,"abstract":"<div><div>The field of endocrine oncology is benefiting from broad advances based on key insights in the pathogenesis of neoplasia. While traditionally regarded as unique and distinct entities from non-endocrine neoplasias, deeper molecular profiling studies of endocrine tumors are now challenging this dogma. In this group of papers, experts from across the field provide their perspectives. Each group focuses on a different endocrine gland which they use as a model that highlights the spectrum of disease behavior. It is hoped that collective reflection on these vignettes will reveal new opportunities that can facilitate more effective detection and therapeutic approaches.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"613 ","pages":"Article 112723"},"PeriodicalIF":3.6,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145878657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toward intelligent hormonal diagnostics: Quantum dots reshaping endocrine disease detection","authors":"Sara Gemini-Piperni ,&nbsp;Temitope Aribigbola ,&nbsp;Marjorie Dardis Murucci ,&nbsp;Zakariyya Muhammad Bello ,&nbsp;Alana da Cunha Goldstein ,&nbsp;Oluwatosin Stella Olayinka ,&nbsp;Tran Nhat Phong Dao ,&nbsp;Rômulo Sperduto Dezonne ,&nbsp;Sunday Amos Onikanni ,&nbsp;Leandro Miranda-Alves","doi":"10.1016/j.mce.2025.112722","DOIUrl":"10.1016/j.mce.2025.112722","url":null,"abstract":"<div><div>Endocrine disorders necessitate diagnostic platforms capable of detecting rapid, low-abundance, fluctuating hormonal signals with high precision. Quantum dot (QD) technology has revolutionized this field by enabling multiplexed, ultrasensitive, and real-time biochemical profiling. Unlike traditional immunoassays limited to single-analyte detection and signal decay, QDs offer exceptional photostability, quantum-level sensitivity, and tunable emission, allowing simultaneous monitoring of various hormonal biomarkers related to thyroid, pancreatic, adrenal, and reproductive dysfunctions. Recent advancements have combined QDs with AI-assisted signal decoding, microfluidics, and wearable biosensor interfaces, creating intelligent systems capable of predicting trends rather than providing static measurements. Functionalized QDs engineered with aptameric, peptidic, or antibody-based recognition domains have shown promising diagnostic capabilities for insulin, estradiol, and thyroid hormones in complex biological samples. As biocompatible QD formulations continue to evolve, their integration with digital health platforms positions them as the next frontier in continuous endocrine monitoring, early disease detection, and personalized hormonal medicine. This review highlights key technological advancements, translational hurdles, and future directions necessary to propel QD-enabled endocrine diagnostics from the laboratory to clinical practice.</div></div>","PeriodicalId":18707,"journal":{"name":"Molecular and Cellular Endocrinology","volume":"613 ","pages":"Article 112722"},"PeriodicalIF":3.6,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145841087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}