Journal of molecular endocrinology最新文献

{"title":"Gestation and Lactation-Dependent Effects of Experimental Hyperthyroidism.","authors":"María Belén Sánchez, María Cecilia Michel Lara, Graciela Alma Jahn, Juan Pablo Mackern-Oberti","doi":"10.1530/JME-25-0198","DOIUrl":"https://doi.org/10.1530/JME-25-0198","url":null,"abstract":"<p><p>Thyroid hormones (T3 and T4) play an essential role in reproductive health and can influence the functions of several endocrine and reproductive tissues, including ovaries, placenta, and mammary glands. Their interactions with other steroid hormones, such as glucocorticoids, estrogens, and progesterone, can alter the balance necessary for reproductive success. Hyperthyroidism can lead to significant endocrine dysregulation that affects multiple reproductive stages. This endocrine disorder causes several alterations in the estrous cycle, restricting conception when the condition is chronic. During pregnancy, hyperthyroidism may lead to several changes associated with preterm birth, which can adversely compromise subsequent lactation. Additionally, during lactation, excess thyroid hormones can impair both the development of the offspring and the extent of lactation by altering the mammary glands and the characteristics of the milk produced. This review explores the endocrine mechanisms behind the effects of experimental hyperthyroidism induced by T4 administration on reproduction. Furthermore, understanding iatrogenic-induced hyperthyroidism is vital for developing therapeutic strategies to mitigate its negative consequences on maternal and neonatal health.</p>","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149194660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hilpda gene expression in steatotic liver is regulated by peroxisome proliferator-activated receptor γ.","authors":"Daisuke Aibara, Takuya Yamashina, Koichi Matsuo, Kimihiko Matsusue","doi":"10.1530/JME-26-0006","DOIUrl":"10.1530/JME-26-0006","url":null,"abstract":"<p><p>Hypoxia-inducible lipid droplet-associated protein (HILPDA) promotes hepatic lipid accumulation. Hilpda gene expression is directly regulated by hypoxia-inducible factors (HIF1A and HIF1B) and the nuclear receptor peroxisome proliferator-activated receptor alpha (PPARα). However, whether the expression of Hilpda is regulated by peroxisome proliferator-activated receptor gamma (PPARγ) in fatty liver remains unclear. In this study, we investigated the role of PPARγ in regulating Hilpda expression in fatty liver. Analysis of publicly available microarray datasets revealed that Hilpda expression is significantly increased in the fatty liver of patients with metabolic dysfunction-associated steatotic liver disease, as well as in obese and type 2 diabetes model ob/ob mice, high-fat diet-fed mice, and mice fed a high-fat, cholesterol-, and fructose-enriched diet, all of which exhibit elevated PPARγ expression. In contrast, Ppara/PPARA expression in the liver remained unchanged in mouse fatty liver models and was decreased in human MASLD liver samples. Hilpda expression in the fatty liver of ob/ob mice was further induced by PPARγ ligand treatment; however, this induction was significantly repressed in liver-specific PPARγ-deficient mice. Complementary in vitro analyses showed that ectopic expression and ligand activation of PPARγ in liver-derived AML-12 cells were sufficient to induce Hilpda transcription, whereas Hif1a and Hif1b were only modestly induced, indicating a minimal contribution of HIF-1 signaling. Overall, our study identifies Hilpda as a key component of the liver PPARγ-driven gene network, highlighting its role as a metabolic effector that adapts to pathological lipid accumulation.</p>","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149111039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteome analysis of different tissues in pregnant women with gestational diabetes and type 1 diabetes mellitus.","authors":"Zeynep Cantürk, Emre Gezer, Gürler Akpınar, Murat Kasap, Ahmet Yiğit Çakıroğlu","doi":"10.1530/JME-26-0064","DOIUrl":"10.1530/JME-26-0064","url":null,"abstract":"<p><p>Gestational diabetes mellitus (GDM) and type 1 diabetes mellitus (T1DM) represent distinct hyperglycemic states during pregnancy. Although proteomic alterations have been described in plasma and placental tissues in GDM, no study has comprehensively compared proteomic changes across multiple relevant tissues in both GDM and T1DM within the same investigation. Tissue samples of omental adipose tissue (OAT), placental tissue (PT), and skeletal muscle tissue (SMT) from pregnant women with GDM and T1DM were obtained during cesarean delivery. Protein extracts were analyzed using two-dimensional gel electrophoresis and difference gel electrophoresis, followed by MALDI-TOF/TOF mass spectrometry for protein identification. Protein-protein interaction analysis was performed using STRING. Selected proteins were further examined by western blotting. We found that carbonic anhydrase 1 (CA1) emerged as the only protein consistently altered in all three tissues. CA1 was upregulated in OAT and PT in GDM but downregulated in the same tissues in T1DM; in SMT, it was downregulated in both groups. Alpha-enolase (ENOA) demonstrated a similar inverse pattern, being upregulated in PT and SMT in GDM but downregulated in T1DM. All of these changes identified by 2DE analysis were statistically significant (P < 0.05). The findings of this study demonstrated that CA1 expression was significantly upregulated in OAT and PT, and ENOA expression was upregulated in PT and SMT. These alterations may reflect differences in the metabolic and hyperglycemic environments of the two conditions and may represent candidate tissue-level markers. Further studies are required to determine their functional and clinical significance.</p>","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148977233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"On the biochemical assessment of maternal thyroid function and thyroid autoantibodies in pregnancy.","authors":"Stine Linding Andersen","doi":"10.1530/JME-26-0060","DOIUrl":"10.1530/JME-26-0060","url":null,"abstract":"<p><p>Thyroid disease is a common endocrine disorder in pregnant women and is important to recognize. Clinical management relies on biochemical assessment of thyroid function and thyroid autoantibodies from a panel of routinely available tests. A challenge regarding biochemical assessment in pregnancy relates to the physiological adaptations that influence the analyses used for diagnosis and monitoring of maternal thyroid disease. The physiological adaptations include increased activity of the thyroid gland, an increase in the levels of binding proteins, and suppression of the immune system, which implies that biochemical test results should be interpreted in the context of pregnancy. This narrative review will discuss the biochemical assessment of thyroid function and thyroid autoantibodies in pregnancy, with a focus on the biochemical methods used and the interpretation of results, including strategies for the establishment of reference intervals. A key implication is that biochemical results obtained in pregnancy should be considered according to the timing of blood sampling and the biochemical method used. This is reflected by recommendations on the use of method- and trimester-specific reference intervals as part of clinical care, but similar considerations apply when thyroid function tests and thyroid autoantibodies are evaluated as part of population monitoring and used for definition of exposure in scientific outcome studies. Future research is encouraged to support the biochemical assessment and interpretation of thyroid function tests and thyroid autoantibodies in pregnancy. Future perspectives include advancements in biochemical methods and in the methodology applied for the establishment of reference intervals or clinical decision limits.</p>","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toxic crossroads: environmental pesticides and their endocrine footprints in global metabolic health.","authors":"Sunday Amos Onikanni, Marjorie Dardis Murucci, Talis Gonçalves da Costa, Omolola Esther Amos, Olawale David Ajayi, Tran Nhat Phong Dao, Basiru Olaitan Ajiboye, Ezekiel Adewole, Sara Gemini Piperni, Leandro Miranda-Alves","doi":"10.1530/JME-25-0183","DOIUrl":"10.1530/JME-25-0183","url":null,"abstract":"<p><strong>Graphical abstract: </strong></p><p><strong>Abstract: </strong>Endocrine-disrupting pesticides (EDPs) exert deleterious effects on the endocrine system, with documented evidence implicating specific pesticides in endocrine disruption, resulting in developmental delays during puberty and thyroid gland dysfunction, thereby increasing susceptibility to metabolic diseases. The disruption of intracellular insulin signaling, which is characterized by redox imbalance, toxicological effects, and pro-inflammatory activity, facilitates cellular adaptation to stress. However, this adaptive response can aberrantly induce a dysfunctional feedback loop characterized by diminished cellular insulin responsiveness, a prevalent feature of metabolic disorders. Despite significant advancements in the scientific understanding of EDPs, substantial knowledge gaps and uncertainties persist, impeding progress toward improved health outcomes. This review highlights current findings on the metabolic toxicity of pesticides in the context of obesity and diabetes, concentrating on crucial signaling pathways and a mechanistic perspective that offers insight into resistance channels as reviewed. These findings enhance our understanding of the potential impacts of EDPs on human health.</p>","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetes compromises DNA damage repair and telomere maintenance in adipose tissue stromal cells, leading to cellular senescence.","authors":"Saiuree Govender, Kelly S Petersen-Ross, Carola U Niesler, Mari van de Vyver","doi":"10.1530/JME-26-0056","DOIUrl":"10.1530/JME-26-0056","url":null,"abstract":"<p><p>Diabetes mellitus (DM) is characterized by chronic metabolic stress that promotes oxidative damage, genomic instability, and premature cellular ageing, with adipose tissue senescence being a pivotal contributor to metabolic dysfunction. Yet, the impact on DNA damage repair (DDR) and telomere maintenance in adipose tissue remains poorly defined. This study investigated DDR capacity, telomere integrity, and the senescence-associated secretory phenotype (SASP) in adipose tissue and adipose tissue-derived stromal cells (ADSCs) under diabetic conditions. Using an obese diabetic (ob/ob) mouse model, we confirmed whole-blood telomere shortening, significant adipose tissue hypertrophy, metabolic dysregulation, and elevated DNA damage, evidenced by increased γH2AX-positive staining. In vitro, ADSCs exposed to a diabetic microenvironment (AGEs and TNFα) exhibited increased reactive oxygen species and DNA damage without a corresponding activation of DDR pathways, as indicated by unchanged PARP1 levels and broad downregulation of key DNA repair genes, including sensors (ATM, ABL1, RAD17) and effectors across the MMR, NER, HR, and NHEJ pathways. This impaired genomic surveillance was accompanied by premature cellular senescence and a significant repression of genes involved in telomere protection (shelterin complex), telomerase activity, and telomere maintenance, together with marked telomere shortening following prolonged exposure. Furthermore, diabetic conditions increased the secretion of pro-inflammatory cytokines, chemokines, and growth factors. Collectively, these findings demonstrate that the diabetic microenvironment is associated with maladaptive DDR responses, telomere dysfunction, cellular senescence, and a pro-inflammatory secretory phenotype. This study highlights compromised genomic maintenance as a potential key mechanism underpinning adipose tissue dysfunction in DM and emphasizes the need for future investigations into the mechanisms underlying dysregulated DDR and telomere biology.</p>","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vagal and splenic influences on the hepcidin-iron homeostasis of lean and hypothalamic obese male rats after induction of anaemia.","authors":"Ellen Carolina Zawoski Gomes, Amanda Rocha Fujita, Marianela Díaz Urrutia, Giovana Fanhani Tessaro, Eveline Cristiane Batista Schmidt Helene, Caroline de Maman Oldra, Sandra Lucinei Balbo, Paulo Correia de Sá, Sabrina Grassiolli","doi":"10.1530/JME-25-0197","DOIUrl":"10.1530/JME-25-0197","url":null,"abstract":"<p><p>The vagus nerve (VN) and spleen are involved in the anti-inflammatory vagal reflex, which influences the metabolic state, with unknown effects on iron metabolism. Here, we evaluate the impact of subdiaphragmatic vagotomy (SV) and splenectomy (SPL) on iron homeostasis in lean and hypothalamic obese male rats after haemolytic anaemia induction. Hypothalamic obesity was induced by monosodium glutamate (MSG; 4 g/kg), administered subcutaneously (s.c.) once every other day from post-natal day 2 (PND2) to PND10. Lean or control (CTRL) rats received equimolar saline (1.25 g/kg; s.c.). On PND60, rats underwent SV, SPL, SV + SPL, or SHAM surgeries. At PND90, haemolytic anaemia was induced by intraperitoneal phenylhydrazine (PHZ; 40 mg/kg). At PND120, the rats were evaluated for adiposity and metabolism, and plasma samples were used to measure iron, hepcidin, total iron-binding capacity (TIBC), and transferrin saturation (TSAT). MSG-obese rats exhibited normal amounts of iron and hepcidin (P > 0.05), associated with increased values of TIBC and TSAT (P < 0.05), compared with CTRL rats. SV reduced adiposity in both CTRL and MSG-obese rats without altering iron levels. However, in MSG-obese animals only, the anti-adiposity effects of SV were accompanied by positive effects on metabolism, especially in association with SPL and PHZ (P < 0.05). SV increased TSAT in MSG-obese animals (P < 0.05). PHZ-induced haemolytic anaemia increased the circulating levels of hepcidin (P < 0.05) in MSG-obese rats, with this response being influenced by the VN and spleen. In conclusion, vagal and splenic mechanisms regulate the adiposity and metabolism of MSG-hypothalamic obese rats, modulating hepcidin and iron transport capacity, independently of fluctuations in plasma iron levels.</p>","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148549505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A literature overview of age- and Tanner stage-specific reference intervals for sex hormones for children aged 0-18 years.","authors":"Anouk Olthof, Anita Boelen, Jacquelien J Hillebrand, Sabine E Hannema, Annemieke C Heijboer","doi":"10.1530/JME-26-0037","DOIUrl":"10.1530/JME-26-0037","url":null,"abstract":"<p><p>This study aims to provide a comprehensive overview of age- and Tanner stage-specific reference intervals (RIs) for testosterone, estradiol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and sex hormone-binding globulin (SHBG) in children and adolescents and to highlight the importance of age- and Tanner stage-specific RIs for clinical practice. A literature review was performed to identify studies reporting RIs on testosterone and estradiol quantified using GC-MS/MS or LC-MS/MS and LH, FSH, and SHBG quantified using immunoassays in healthy individuals aged 0-18 years, categorized by age and/or Tanner stage. Sample sizes were evaluated according to the Clinical Laboratory Standards Institute (CLSI) guideline CLSI EP28-A3c, with ≥120 samples per group being acceptable, 39-119 samples being poor, and ≤38 samples being unacceptable. Analytical methods and statistical approaches were carefully documented. Fourteen studies were included for testosterone, seven for estradiol, thirteen for LH and FSH, and nine for SHBG. The results revealed considerable variability in the availability and quality of RIs, with many studies lacking adequate sample size or appropriate partitioning. Testosterone, estradiol, LH, and FSH RIs demonstrated significant changes during mini-puberty and puberty, with clear sex-specific patterns. SHBG RIs fluctuated throughout childhood and adolescence. This literature review demonstrates that RIs for HPG axis hormones show significant changes during mini-puberty and puberty, although data using appropriate analytical methods, using sufficient sample sizes, and reporting on age categories, Tanner stage, and menstrual cycle phase are scarce. Robust age- and Tanner stage-specific RIs are essential to improve diagnostic accuracy and individualized care in children and adolescents.</p>","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13506540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148679007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Caspase-8 as a candidate mediator associated with everolimus resistance in neuroendocrine tumors.","authors":"Cristina Grassi, Miriam Bondi, Giulia Albanese, Alessandro Zerbi, Silvia Uccella, Erika Peverelli, Giovanna Mantovani, Elisabetta Lavezzi, Giuseppe Marulli, Andrea Gerardo Antonio Lania, Eleonora Vitali","doi":"10.1530/JME-25-0206","DOIUrl":"10.1530/JME-25-0206","url":null,"abstract":"<p><p>Everolimus, an mTORC1 inhibitor, is approved for treating pancreatic and lung neuroendocrine tumors (NETs), yet acquired resistance limits its long-term efficacy. The molecular mechanisms underlying resistance and potential strategies to overcome it remain poorly defined. RNA sequencing was performed in everolimus-sensitive and everolimus-resistant QGP-1 pancreatic NET cells (QS and QR, respectively) to identify transcriptional changes associated with everolimus resistance. Key differentially expressed genes were validated in QGP-1, H727 lung NET cells, and patient-derived Pa-NET cells using RT-qPCR. The potential functional involvement of caspase-8 (CASP8) was investigated pharmacologically using the preferential CASP8 inhibitor Z-IETD-FMK, alone or in combination with everolimus, by evaluating effects on cell viability and CASP activity. Differential expression analysis identified 292 genes significantly dysregulated in QR versus QS cells, including CASP8, A2M, MGP, PTGS1, and IGFBP5. Enrichment analysis highlighted pathways related to ECM remodeling, neuroactive ligand-receptor interactions, and GPCR signaling. Validation in H727 cells and primary Pa-NET samples showed some conserved transcriptional changes, with CASP8 upregulation emerging as a particularly consistent alteration. CASP8 inhibition reduced viability in both QS and QR cells, while combined Z-IETD-FMK and everolimus treatment produced the greatest decrease in QS viability and was associated with reduced CASP3/7 activity. Our study identifies CASP8 as a candidate mediator associated with everolimus resistance in NETs, together with alterations in ECM remodeling and receptor signaling. These findings support further investigation of CASP8-targeting strategies, particularly in combination with mTOR inhibition, as a potential approach to enhance therapeutic efficacy.</p>","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148794474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BAMBI acts as a molecular switch to determine the cell fate of C2C12 myoblasts.","authors":"Xiangping Yao, Liwei Xie","doi":"10.1530/JME-25-0169","DOIUrl":"10.1530/JME-25-0169","url":null,"abstract":"<p><p>Myogenesis is a tightly regulated process by a cascade of well-coordinated events and pathways. In addition to the known myogenic regulatory factor (MRF) family, including Myf5, MyoD, myogenin, and MRF4, our previous study identified that BAMBI is involved in muscle regeneration and siRNA-mediated BAMBI knockdown impairs C2C12 myoblast differentiation. However, the potential role of BAMBI in determining cell lineage and fate specification in C2C12 myoblasts remains unexplored. In this study, we analyzed the RNA-seq data and discovered that BAMBI expression was dynamically regulated during the proliferation and differentiation period of C2C12 myoblasts. By establishing a cell line with the loss of function and gain of function of BAMBI in C2C12 myoblasts, we demonstrated that BAMBI deletion totally abrogated myogenic differentiation of C2C12 myoblast cells. In addition, loss of BAMBI converts C2C12 myoblasts to brown adipocytes through downregulation of MyoD and upregulation of Prdm16. Conversely, BAMBI overexpression strikingly enhanced myogenic differentiation of C2C12 myoblasts by upregulating MyoD expression. Taken together, our results establish that BAMBI is a vital myogenic factor involved in myoblast differentiation and a key regulator governing the balance between myogenic and adipogenic lineages in C2C12 myoblast cells.</p>","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}