Frontiers in Endocrinology最新文献

{"title":"Correction: Sociodemographic and clinical predictors of malignancy in thyroid nodules: a systematic review and meta-analysis.","authors":"Vanessa Neto, Catarina Leitão, Cláudia Martins, Margarida Fardilha, Maria Teresa Herdeiro, Alexandra Nunes","doi":"10.3389/fendo.2026.1981738","DOIUrl":"https://doi.org/10.3389/fendo.2026.1981738","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fendo.2026.1885823.].</p>","PeriodicalId":12447,"journal":{"name":"Frontiers in Endocrinology","volume":"17 ","pages":"1981738"},"PeriodicalIF":5.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophages and immunometabolism in diminished ovarian reserve: pathological features and therapeutic implications.","authors":"Bingxia Li, Jia Zhang, Quansheng Wu, Xiaohua Zhang","doi":"10.3389/fendo.2026.1883984","DOIUrl":"https://doi.org/10.3389/fendo.2026.1883984","url":null,"abstract":"<p><p>Diminished ovarian reserve (DOR) is a prevalent reproductive endocrine disorder that significantly impairs female fertility. While traditional research has emphasized intrinsic oocyte defects, growing evidence highlights the ovarian immune microenvironment-specifically macrophages-as a critical regulator of follicular fate and reserve maintenance. Nevertheless, the mechanisms by which macrophage dysfunction drives DOR remain incompletely understood, and the interplay between chronic inflammation and macrophage metabolic reprogramming has yet to be systematically elucidated. This narrative review synthesizes literature from immunology, metabolism, and reproductive medicine, framing current evidence as established findings, putative mechanisms, and emerging hypotheses. The key findings are threefold: 1) macrophage polarization imbalance, which is marked by sustained M1 activation and impaired M2 function, constitutes a core pathological feature of DOR; 2) this imbalance is driven by metabolic reprogramming-specifically, metabolic inflexibility in M1 (persistent glycolytic commitment) and suppressed oxidative phosphorylation in M2-which links inflammaging to ovarian fibrosis and follicular depletion; and 3) pharmacological modulation of macrophage immunometabolism (e.g., AMPK/PPARγ activators, LXR agonists, and itaconate) and engineered delivery platforms (e.g., exosomes and targeted nanocarriers) hold preclinical promise. This review establishes an \"immunometabolic axis\" framework that integrates macrophage polarization, metabolic dysregulation, and ovarian reserve loss, advancing the understanding of DOR pathogenesis and informing precision interventions.</p>","PeriodicalId":12447,"journal":{"name":"Frontiers in Endocrinology","volume":"17 ","pages":"1883984"},"PeriodicalIF":5.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early prediction of gestational diabetes mellitus using deep learning applied to routinely collected clinical data.","authors":"Gabriel Cubillos, Max Monckeberg, Sebastian E Illanes, Claudio A Perez","doi":"10.3389/fendo.2026.1941799","DOIUrl":"https://doi.org/10.3389/fendo.2026.1941799","url":null,"abstract":"<p><strong>Background: </strong>Prediction of gestational diabetes mellitus (GDM) in early pregnancy enables timely, targeted interventions to reduce risks for both the mother and fetus. We aimed to improve early GDM prediction and clinical risk stratification using a novel deep learning (DL) approach that transforms tabular clinical data into images using a genetic algorithm.</p><p><strong>Methods: </strong>A dataset of 1,611 pregnancies was used. The dataset contained routinely collected early-pregnancy data, including clinical measurements, blood tests, and medical history. A novel method to transform tabular data into images was applied to enable the use of deep learning models for GDM prediction. A genetic algorithm optimized the spatial arrangement of variables during image generation by determining their spatial positions. Interpretability was assessed using gradient-weighted class activation mapping (Grad-CAM) to identify variables the model preferentially attended to for positive and negative predictions.</p><p><strong>Results: </strong>Multiple model configurations were evaluated by varying the spatial arrangement of variables within the transformation. Prioritizing high sensitivity, one model achieved an accuracy of 0.86, sensitivity of 0.82, specificity of 0.87, and an AUC-ROC of 0.83. Another model achieved an accuracy of 0.79, sensitivity of 0.92, specificity of 0.77, and an AUC-ROC of 0.85. Compared with previously published machine learning models using the same dataset, our approach demonstrated improved performance. Our best models increased specificity by an average of 13.93 percentage points compared with traditional ML models at matched sensitivity levels, thereby reducing false-positive classifications that may lead to additional clinical evaluation. Grad-CAM analysis revealed that attention patterns of the model aligned with established clinical risk factors for GDM, with first trimester fasting glycemia and parity preferentially attended for positive predictions and maternal weight for negative predictions.</p><p><strong>Conclusions: </strong>This study demonstrates that transforming tabular clinical data into image representations, optimized using a genetic algorithm, improves early GDM prediction. Representing tabular variables as images enables more effective application of DL models, which have demonstrated enhanced pattern recognition in image-based tasks compared with traditional machine learning methods. Performance improvements over state-of-the-art approaches were achieved. Accurate DL models can be developed using a limited number of input variables, supporting early identification of women at increased risk of GDM and facilitating timely clinical management.</p>","PeriodicalId":12447,"journal":{"name":"Frontiers in Endocrinology","volume":"17 ","pages":"1941799"},"PeriodicalIF":5.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13677491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endocrine-disrupting chemicals in male reproductive health: exposure risks, reproductive toxicity and emerging perspectives.","authors":"Dongyue Ma, Qingjiang Yang, Jun Guo, Wenguang Zhou, Chen Huang, Xiangping Sun","doi":"10.3389/fendo.2026.1956000","DOIUrl":"https://doi.org/10.3389/fendo.2026.1956000","url":null,"abstract":"<p><p>Male reproductive health represents a growing global health challenge, and increasing evidence highlights the contribution of environmental exposures to declining male reproductive function. Endocrine-disrupting chemicals are widespread environmental contaminants that interfere with endocrine regulation and have been associated with impaired semen quality, hormonal imbalance and testicular dysfunction. Here, we summarize current advances in understanding EDC-induced male reproductive toxicity, focusing on major chemical classes, including bisphenols, phthalates, pesticides, per- and polyfluoroalkyl substances and heavy metals. We discuss the interconnected mechanisms underlying reproductive impairment, including disruption of the hypothalamic-pituitary-gonadal axis, altered steroidogenesis, oxidative stress, mitochondrial dysfunction, blood-testis barrier disruption, immune dysregulation and epigenetic reprogramming. Importantly, emerging evidence from developmental origins of health and disease perspectives indicates that exposure during critical developmental windows may establish persistent molecular alterations, influencing reproductive outcomes across the life course. In addition, the metabolic effects of certain EDCs, including obesity and metabolic dysfunction, may further exacerbate male reproductive impairment. Given that human exposure occurs predominantly in the form of complex chemical mixtures, future research should integrate exposomics, multi-omics approaches and longitudinal cohorts to clarify causal relationships and identify susceptible populations. Such advances will be essential for developing precision environmental health strategies to preserve male reproductive function.</p>","PeriodicalId":12447,"journal":{"name":"Frontiers in Endocrinology","volume":"17 ","pages":"1956000"},"PeriodicalIF":5.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678584/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-term clinical outcomes in females with precocious puberty treated with gonadotropin-releasing hormone analogues.","authors":"Nahla Khawaja, Khalid Karaki, Mohammad K Ruba'i, Yousef Khader, Arwa Kinani, Oraib Farahid, Mohammed El-Khateeb, Omar Ali, Abdulrahman Abujbara, Laith Hyasat, Kamel Ajlouni","doi":"10.3389/fendo.2026.1911743","DOIUrl":"https://doi.org/10.3389/fendo.2026.1911743","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate long-term anthropometric, metabolic, reproductive, and bone mineral density (BMD) outcomes in girls with central precocious puberty (CPP) treated with Gonadotropin-Releasing Hormone analogues (GnRHa).</p><p><strong>Methods: </strong>In this retrospective cohort with cross-sectional follow-up assessment, 82 of 265 eligible females (30.9%) with central precocious puberty or central hypothalamic-pituitary-gonadal axis activation who had received GnRHa participated in long-term evaluation. Anthropometric outcomes, insulin sensitivity indices (HOMA-IR and QUICKI), hormonal profile, BMD, and reproductive outcomes including polycystic ovary syndrome (PCOS) were assessed. Analyses used available cases for each outcome; missing values were not imputed.</p><p><strong>Results: </strong>The mean age at final evaluation was 17.61 ± 4.3 years, and mean GnRHa treatment duration was 3.14 ± 1.9 years. Mean height at final follow-up was 159.85 ± 6.5 cm; the mean difference from baseline predicted adult height was 1.98 cm (95% CI, -0.37 to 4.34; P = 0.097). The distribution of BMI categories did not change significantly from baseline to final follow-up. Mean HOMA-IR and QUICKI were 3.76 ± 1.82 and 0.319 ± 0.025, respectively; among adults, 14/28 (50.0%) met each prespecified adult-derived threshold for reduced insulin sensitivity. PCOS was identified in 15/67 participants (22.4%). Mean lumbar and femoral BMD Z-scores were -0.25 ± 1.23 and -0.55 ± 1.03, respectively.</p><p><strong>Conclusions: </strong>Among participants who completed long-term follow-up, attained height was comparable at the group level with predicted adult and mid-parental height, and mean BMD Z-scores were within age- and sex-referenced ranges. PCOS and PCOS-related features were observed, while insulin sensitivity indices were associated with adiposity. Because only 30.9% of eligible patients participated and there was no untreated comparison group, these findings describe the evaluated cohort and should not be interpreted as causal effects of GnRHa treatment.</p>","PeriodicalId":12447,"journal":{"name":"Frontiers in Endocrinology","volume":"17 ","pages":"1911743"},"PeriodicalIF":5.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13677348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beta-cell replacement for type 1 diabetes: integrating cell products, engraftment and immune protection.","authors":"Lan Chen, Xinhao Hu, Chen Zheng, Qi Huang, Jiani Xu, Xiongbin You, Chenfang Wang","doi":"10.3389/fendo.2026.1981945","DOIUrl":"https://doi.org/10.3389/fendo.2026.1981945","url":null,"abstract":"<p><p>Beta-cell replacement aims to restore endogenous, glucose-responsive insulin secretion in type 1 diabetes. Donor-islet transplantation has shown that this approach can improve glycaemic control and prevent severe hypoglycaemia. Its wider use is limited by donor supply, early graft loss and chronic systemic immunosuppression. Pluripotent stem cells provide a renewable source of pancreatic progenitors and differentiated islet products. Recent clinical studies have reported C-peptide secretion and insulin independence in some recipients. However, cell supply is only one part of the problem. Product maturity, graft composition, implantation site, vascular support, immune injury and manufacturing quality all affect outcome. This review examines these factors as parts of one treatment system. It compares donor islets, stem-cell-derived products and islet-like organoids, then evaluates delivery and immune-protection strategies. It also considers clinical endpoints, patient selection and safety. We define functional cure as durable endogenous insulin secretion with physiological benefit at an acceptable total treatment burden. Current evidence provides early evidence of clinical activity and, in selected recipients, clinically meaningful efficacy. However, the available studies involve highly selected participants, small cohorts and/or systemic immunosuppression. No platform has yet combined durable function, immune control, scalable production and acceptable long-term safety.</p>","PeriodicalId":12447,"journal":{"name":"Frontiers in Endocrinology","volume":"17 ","pages":"1981945"},"PeriodicalIF":5.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149227667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic memory in diabetic complications: evidence for persistent cellular states and limits of therapeutic reversal.","authors":"Yulan Cai, Shuangyu He, Feng Zeng, Chuyu Liu","doi":"10.3389/fendo.2026.1954392","DOIUrl":"https://doi.org/10.3389/fendo.2026.1954392","url":null,"abstract":"<p><p>Metabolic memory is defined here as an exposure-history-dependent cellular phenotype that persists beyond immediate carry-over after verified withdrawal of the initiating exposure, principally high glucose and is accompanied by a specified functional impairment or an altered response to the same defined secondary stimulus. This operational definition separates cellular memory from clinical legacy effects, continuing local stimulation and residual structural injury. We critically examine evidence from longitudinal clinical studies, human biospecimens, animal models and controlled cell experiments, distinguishing molecular persistence, measured signaling activity, causal maintenance and treatment-free durability. DCCT/EDIC and UKPDS establish lasting benefits of earlier glycemic management but do not independently identify cellular memory as the mechanism. Experimental evidence supports selected endothelial redox circuits, epigenetic regulation and hematopoietic progenitor training; human causal evidence is substantially more limited. Persistent chromatin marks do not necessarily imply continuously active signaling, and latent priming may become apparent only after rechallenge. In kidney, cardiovascular, retinal and wound disease, candidate cellular memory coexists with hypoxic or inflammatory niches and structural loss. Pancreatic β-cell plasticity is considered a comparative endocrine model rather than an established complication-memory circuit. The proposed interactions among epigenetic, mitochondrial, metabolic and inflammatory mechanisms remain a framework supported by selected local feedback loops, not a universally demonstrated network. Therapeutic evidence is organized into prevention, modification or suppression of established abnormalities, and sustained molecular and functional recovery after treatment cessation after intervention withdrawal. The latter remains unestablished in patients for the mechanisms reviewed. Early glycemic and multifactorial management remains essential, while mechanistic translation requires explicit recovery, perturbation and post-treatment follow-up designs.</p>","PeriodicalId":12447,"journal":{"name":"Frontiers in Endocrinology","volume":"17 ","pages":"1954392"},"PeriodicalIF":5.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glucagon-like peptide-1 receptor agonists and aesthetic surgery: perioperative safety, timing, durability and body composition.","authors":"Richa Chaturvedi, Kuldeep Singh, Rameshwari R Chakole, Bhupesh K Yadav, Juli Dhameliya, Deepali Joshi","doi":"10.3389/fendo.2026.1969433","DOIUrl":"https://doi.org/10.3389/fendo.2026.1969433","url":null,"abstract":"<p><p>Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and dual incretin agonists have transformed the management of obesity and type 2 diabetes and are rapidly reshaping the population seeking aesthetic surgery. By producing double-digit percentage weight loss, these agents expand eligibility for elective procedures while generating new patterns of skin redundancy, soft-tissue laxity, and facial volume depletion that drive demand for body contouring and facial rejuvenation. At the same time, incretin therapy introduces distinct perioperative considerations: delayed gastric emptying with possible pulmonary aspiration in symptomatic patients, gastrointestinal adverse effects that peak during dose escalation, loss of lean mass with rapid weight reduction, nutritional inadequacy during profound appetite suppression, and frequent weight regain after drug discontinuation, which threatens the durability of surgical results. This mini-review synthesizes current evidence on the mechanisms of GLP-1 RAs relevant to the reconstructive surgical patient, summarizes the evolving guidance from anesthesia societies, moving from blanket preoperative withholding to individualized risk stratification, reviews emerging outcome data on body contouring in GLP-1 RA users, and discusses body composition, sarcopenia risk, and nutritional optimization. We propose a pragmatic framework, anchored in weight stability and symptom burden, for timing elective aesthetic procedures relative to GLP-1 RA initiation, escalation, and maintenance, along with a multidisciplinary perioperative algorithm that links the endocrinologist, plastic surgeon, and anesthesiologist. As incretin-based pharmacotherapy expands globally, coordinated endocrine-surgical-anesthetic care will be essential to maximize safety, functional recovery, and patient satisfaction in the GLP-1 era.</p>","PeriodicalId":12447,"journal":{"name":"Frontiers in Endocrinology","volume":"17 ","pages":"1969433"},"PeriodicalIF":5.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endocrine determinants of MASLD: mechanisms and therapeutic targets.","authors":"Richa Chaturvedi, Anu Mathew, Aprajita Pradhan, Monika Goyal, Monika Sharma, Varsha Kachroo, Chhavi Agrawal, Aishwarya Krishnamurthy, Surabhi Atreja, Ashish Atreja","doi":"10.3389/fendo.2026.1967494","DOIUrl":"https://doi.org/10.3389/fendo.2026.1967494","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) affects approximately 30% of adults worldwide, yet is still framed largely as a hepatological disorder despite being driven substantially by endocrine and metabolic dysfunction. This review proposes a unified endocrine framework organised around seven hormonal axes, presenting each in terms of molecular pathogenesis, clinical presentation, and therapeutic implications. Insulin resistance is the central driver, coupling chronic caloric excess to hepatic <i>de novo</i> lipogenesis through selective hepatic insulin resistance, although genetic variants in <i>PNPLA3</i> and <i>TM6SF2</i> can uncouple steatosis from metabolic risk. Adipose tissue dysfunction contributes through adipocyte senescence, adipokine imbalance, and inflammatory adipose-liver signalling. Reduced hepatic thyroid hormone sensitivity, even in euthyroid individuals, predicts steatosis and fibrosis and underpins the first approved liver-directed therapy. Gonadal steroids exert sexually dimorphic effects, with testosterone deficiency, menopausal oestrogen loss, and polycystic ovary syndrome representing distinct risk states. Glucocorticoid dysregulation is stage-dependent, shifting from enhanced hepatic cortisol clearance in steatosis to local amplification in steatohepatitis. The gut-liver-endocrine axis, encompassing incretin, bile acid, and fibroblast growth factor signalling, has proved the most therapeutically tractable. Reduced GH/IGF-1 signalling, whether from pituitary disease or obesity-induced functional suppression, promotes both steatosis and fibrogenesis. Biological sex and life-course influences spanning developmental programming and ageing further modify these determinants. Two agents, resmetirom and semaglutide, now have US FDA accelerated approval for noncirrhotic MASH with moderate-to-advanced fibrosis, supporting the principle that correcting axis-specific endocrine dysfunction can produce measurable hepatic benefit; however, both approvals are accelerated and await confirmatory outcome data, while others remain investigational. An endocrine framework offers both a coherent account of pathogenesis and a rational basis for biomarker-guided, phenotype-targeted therapy.</p>","PeriodicalId":12447,"journal":{"name":"Frontiers in Endocrinology","volume":"17 ","pages":"1967494"},"PeriodicalIF":5.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Implementation of guideline-recommended organ-protective therapy in people with type 2 diabetes and cardiovascular disease, heart failure, or kidney disease: real-world evidence from a German University Hospital.","authors":"Karzan Suliman, Young Hee Lee-Barkey, Alexander Brehmer, Bernd Stratmann, Jasmin M Klose, Tim Lenfers, Jens Kleesiek, Susanne Reger-Tan, Julius Keyl","doi":"10.3389/fendo.2026.1954561","DOIUrl":"https://doi.org/10.3389/fendo.2026.1954561","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fendo.2025.1736984.].</p>","PeriodicalId":12447,"journal":{"name":"Frontiers in Endocrinology","volume":"17 ","pages":"1954561"},"PeriodicalIF":5.7,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13679133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}