Anat Ben-Shlomo, Michelle Koh, Sarah Kremen, Jeffrey Wertheimer
{"title":"Cognitive Assessment in Adults With Adrenal Cortisol Insufficiency: Challenges and Opportunities.","authors":"Anat Ben-Shlomo, Michelle Koh, Sarah Kremen, Jeffrey Wertheimer","doi":"10.1210/endrev/bnaf029","DOIUrl":"10.1210/endrev/bnaf029","url":null,"abstract":"<p><p>Adults with adrenal cortisol insufficiency (ACI) often report cognitive dysfunction, especially in memory processing and executive function. Only a few studies have objectively compared cognitive function as the primary outcome between patients with ACI and controls, and these efforts have yielded inconsistent results. In this review, we examine the challenges facing researchers studying cognitive function in adult patients with ACI. We consider the effect of dysregulated cortisol on cognition in patients with ACI, and the inability of current guideline-recommended glucocorticoid (GC) treatment regimens to accurately reproduce circadian and ultradian cortisol secretion rhythms. Factors that contribute to inter- and intra-individual response to GC are presented; the indirect effects of ACI comorbidities, complications, and symptoms on cognitive dysfunction are reviewed; and obstacles to employing neurocognitive testing are identified. Finally, we outline potential approaches to studying cognition in ACI using well-designed studies that account for the complexities and gaps in ACI research.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":"24-51"},"PeriodicalIF":22.0,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12795706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144947170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Marta Araujo-Castro,Cristina Lamas,Elisabeth Nowak,John Newell-Price,Martin Reincke,Frederic Castinetti
{"title":"Update and practical recommendations for the use of medical treatment of Cushing´s syndrome.","authors":"Marta Araujo-Castro,Cristina Lamas,Elisabeth Nowak,John Newell-Price,Martin Reincke,Frederic Castinetti","doi":"10.1210/endrev/bnaf042","DOIUrl":"https://doi.org/10.1210/endrev/bnaf042","url":null,"abstract":"Medical treatment of hypercortisolism may be necessary for a high proportion of patients with Cushing´s syndrome (CS), including those who are not candidates for curative surgery. It may also be used in the presurgical period when hypercortisolism is severe, and as long-term treatment following surgical failure or recurrence after surgery, or whilst waiting for the effects of pituitary radiation in Cushing´s disease (CD). Currently available medical treatments include adrenal steroidogenesis inhibitors that block cortisol secretion (ketoconazole, levoketoconazole, metyrapone, osilodrostat, mitotane, and etomidate), drugs that modulate pituitary ACTH secretion (pasireotide and cabergoline), and drugs that block peripheral glucocorticoid receptors (mifepristone). In addition, there are other medical treatments in development that target pituitary signaling pathways, ACTH or its adrenal receptor, or the conversion of cortisol from cortisone by 11ßHSD1. Steroidogenesis inhibitors can be administered using either a titration or a block-and-replace approach. Titration requires adjusting the daily drug dose with the aim of normalizing circulating cortisol levels, while the block-and-replace strategy uses higher drug doses to fully suppress endogenous cortisol production, followed by glucocorticoid supplementation. In this review, we summarize the main indications for medical treatment in CS, the mechanism of drug action, efficacy, recommended doses, and safety of the currently available drugs, as well as potential future treatments. We also discuss titration and block-and-replace approaches for control of hypercortisolism and provide recommendations for the use and monitoring of medical treatment in CS, including patients with endogenous hypercortisolism in special situations such as pregnancy, cyclic CS and mild autonomous cortisol secretion.","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":"105 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145897511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shalender Bhasin,Chengzhi Wang,Mohan S Chandra,Thiago Gagliano-Jucá,Ravi Jasuja
{"title":"Mechanisms of Testosterone's Anabolic Effects on Muscle and Function: Controversies and New Insights.","authors":"Shalender Bhasin,Chengzhi Wang,Mohan S Chandra,Thiago Gagliano-Jucá,Ravi Jasuja","doi":"10.1210/endrev/bnaf041","DOIUrl":"https://doi.org/10.1210/endrev/bnaf041","url":null,"abstract":"Testosterone treatment increases muscle mass, maximal voluntary muscle-strength, aerobic capacity, and some measures of physical function. Activational and epigenetic mechanisms by which androgens improve muscle mass and physical performance and how to apply these anabolic effects to treat functional limitations associated with aging and disease remain incompletely understood. Testosterone treatment induces hypertrophy of type 1 and 2 muscle fibers, and increases muscle progenitor cell numbers by promoting differentiation of mesenchymal progenitor cells into myogenic lineage by an androgen receptor (AR)-mediated pathway. Liganded AR binds to β-catenin, translocates into nucleus where it binds TCF4 and upregulates follistatin that blocks signaling through TGFβ-pathway to promote myogenesis and inhibit adipogenesis. Testosterone increases myoblast proliferation by stimulating polyamine biosynthesis. Stimulation of GH and IGF-1 secretion, intramuscular IGF1-receptor, and muscle protein synthesis, and inhibition of muscle atrophy genes further contribute to testosterone's anabolic effects. Testosterone improves muscle bioenergetics by increasing erythrocytes, oxygen availability, tissue blood flow, and mitochondrial mass and quality. Testosterone increases blood flow by nongenomic mechanisms involving NO production, and calcium and potassium channels in vascular smooth muscle. The conversion of testosterone to 5α-dihydrotestosterone is not required for mediating its anabolic effects. Mechanisms of testosterone's sexually-dimorphic epigenetic and tissue-specific activational effects; and roles of α-keto reductase and steroid 5α-reductase, one-carbon and polyamine metabolism in testosterone's actions remain poorly understood. Strategies to translate testosterone-induced muscle mass and strength gains into patient-important improvements in functional performance and health outcomes are needed to enable its clinical applications to treat functional limitations associated with aging and disease.","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":"376 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Javad Anjom-Shoae,Simon Veedfald,Arthur D Conigrave,Michael Horowitz,Christine Feinle-Bisset
{"title":"Calcium-sensing receptor regulation of gastrointestinal hormone secretion.","authors":"Javad Anjom-Shoae,Simon Veedfald,Arthur D Conigrave,Michael Horowitz,Christine Feinle-Bisset","doi":"10.1210/endrev/bnaf040","DOIUrl":"https://doi.org/10.1210/endrev/bnaf040","url":null,"abstract":"The interaction of dietary nutrients with chemoreceptors in the gastrointestinal tract after a meal stimulates the secretion of gut hormones, which trigger the key processes of digestion and absorption, and also regulate energy intake and postprandial glycaemia. One of these receptors, first recognised for its capacity to gauge extracellular calcium (Ca2+), is the calcium-sensing receptor (CaSR). Subsequent to its cloning, the CaSR was found to sense not only Ca2+, but also L-amino acids (AAs) and, based on solved protein structures, distinct binding sites have been reported for Ca2+ ions and the aromatic AA, L-tryptophan (L-Trp). In the stomach and small intestine, the CaSR is expressed in enteroendocrine cells, and a substantial body of preclinical work has demonstrated that it mediates gut hormone secretion in response to L-Trp and another aromatic AA, L-phenylalanine (L-Phe), and that extracellular Ca2+ promotes these effects. In humans, intraluminal administration of L-Trp or L-Phe increases plasma levels of gut hormones, associated with reductions in both energy intake and the plasma glucose response to a subsequent meal. In addition, co-administration of Ca2+ enhances the effect of L-Trp to increase plasma levels of gut hormones (including cholecystokinin, glucagon-like peptide-1 and peptide YY) and reduce energy intake. These observations have implications for the development of novel nutrient-based management strategies for obesity and type 2 diabetes. This review considers preclinical and clinical evidence that CaSR activators, including extracellular Ca2+ as well as the aromatic AAs, L-Trp and L-Phe, stimulate gut hormones and lower both energy intake and postprandial glycaemia.","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":"25 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145644993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nanna S Svensson, Tabia Volqvartz, Anna Louise Vestergaard, Esben T Vestergaard, Agnete Larsen, Pinar Bor
{"title":"Effects of Maternal Vitamin D Supplementation on Childhood Health.","authors":"Nanna S Svensson, Tabia Volqvartz, Anna Louise Vestergaard, Esben T Vestergaard, Agnete Larsen, Pinar Bor","doi":"10.1210/endrev/bnaf034","DOIUrl":"10.1210/endrev/bnaf034","url":null,"abstract":"<p><p>Vitamin D deficiency during pregnancy is associated with an increased risk of health issues in the offspring. Accordingly, recent Endocrine Society guidelines strongly support supplementation in pregnancy, also underlining that without consensus on optimal maternal vitamin D levels, routine screening is currently irrelevant. Knowledge of organ-specific effects of vitamin D and its association with maternal vitamin D status may aid in optimizing vitamin D supplementation. This systematic review outlines the proposed next-generation effects of vitamin D supplementation ≥400 IU/d and explores whether such effects are attributed to a specific maternal vitamin D level obtained during pregnancy. A systematic literature search was conducted in PubMed and Embase according to the PRISMA guidelines, focusing on health outcomes from 10 days postpartum and beyond. Of the 2383 screened articles, 38 were included. In 11 of 16 studies, vitamin D supplementation reduced respiratory tract infections in the first years of life. Growth or bone development benefits were observed in 6 of 12 studies. Positive effects on neurodevelopment and reduced autoimmune risk (diabetes-related antibodies) were noted, although further research is needed to determine the role of vitamin D. Very few studies have measured vitamin D concentrations, but even 1600 IU/d supplementation was associated with high frequency of infant vitamin D insufficiency. Current recommendations may not ensure sufficient vitamin D levels at birth, among others, increasing the risk of early-life infections. Further studies linking maternal and infant vitamin D levels to specific outcomes would aid in personalized nutritional advice during pregnancy and improve next-generation health.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":"922-953"},"PeriodicalIF":23.9,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12640715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145354067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Leonard Girnita, Joseph A M J L Janssen, Terry J Smith
{"title":"G Protein-coupled and Membrane Tyrosine Kinase Receptor Relationships Yield Therapeutic Opportunities.","authors":"Leonard Girnita, Joseph A M J L Janssen, Terry J Smith","doi":"10.1210/endrev/bnaf019","DOIUrl":"10.1210/endrev/bnaf019","url":null,"abstract":"<p><p>The aim of this review is to describe the complex evolutionary processes that have integrated signaling cascades associated with 2 structurally and mechanistically dissimilar receptor families: G protein-coupled receptors (GPCRs) and membrane-spanning tyrosine kinase receptors (RTKs). Precision medicine, employing advanced personalized therapeutic strategies, requires better understanding of multiple mechanisms governing both normal and pathological cell regulation. The functional overlap of GPCRs and RTKs exhibits complex interactions. GPCRs canonically activate signaling through their interactions with G proteins; however, they can also initiate G protein-independent signaling through interactions with β-arrestin 1/2. In contrast to the GPCRs, RTK canonical signaling is initiated with ligand-dependent receptor kinase-mediated phosphorylation of specific intrinsic tyrosine substrates. This, in turn, activates multiple intracellular pathways. Despite these distinguishing characteristics, GPCRs and RTKs might have a common evolutionary origin. This shared ancestry potentially explains why GPCRs and RTKs can behave as functional RTK/GPCR hybrids by \"borrowing\" from each other's signaling toolbox. Intermingling of these cell surface receptors can result in noncanonical receptor transactivation/inactivation, trafficking, and signaling. Several mechanisms for heterogeneous receptor crosstalk have been proposed, including receptor protein/protein interactions and sharing docking, scaffolding, and downstream effectors. Recent identification of these signaling complexities has revealed unanticipated feedback loops and patterns of downstream target gene activation. In sum, recognizing these biological complexities should facilitate novel approaches to high-specificity therapeutic targeting.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":"810-837"},"PeriodicalIF":23.9,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Obesity and Exercise: New Insights and Perspectives.","authors":"Natasha Maria James, Kristin I Stanford","doi":"10.1210/endrev/bnaf017","DOIUrl":"10.1210/endrev/bnaf017","url":null,"abstract":"<p><p>Obesity is increasing rapidly worldwide and is projected to affect approximately half the US population by the year 2035. Obesity is a complex condition, and individuals who have obesity are at greater risk for developing associated metabolic diseases such as type 2 diabetes (T2D), metabolic dysfunction-associated steatohepatitis (MASH), and cardiovascular diseases (CVD). Understanding the underlying factors which contribute to obesity and that impact key molecular mechanisms of metabolic organs such as adipose tissue, liver, and muscle is crucial for combating the disease. Exercise is a well-established measure to prevent or mitigate the adverse consequences of obesity, with several beneficial effects to whole-body metabolism and adaptations to metabolic tissues. This review explores the impact of obesity on the development of metabolic diseases. Specifically, we will discuss: how obesity alters metabolic function and the potential benefits of exercise; the specific effects of obesity and exercise on muscle, adipose tissue, and liver; and potential effects of pharmacotherapeutics or bariatric surgery in combination with exercise.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":"763-789"},"PeriodicalIF":23.9,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12640717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anna Claire G Fernandez, Sanika Pelnekar, Joshua F Robinson, Gary M Shaw, Amy M Padula, Tracey J Woodruff, Linda C Giudice
{"title":"Climate Change and Reproductive Health.","authors":"Anna Claire G Fernandez, Sanika Pelnekar, Joshua F Robinson, Gary M Shaw, Amy M Padula, Tracey J Woodruff, Linda C Giudice","doi":"10.1210/endrev/bnaf026","DOIUrl":"10.1210/endrev/bnaf026","url":null,"abstract":"<p><p>Climate change is a major threat to the world's population and is due to global warming from human activities that increase atmospheric greenhouse gas levels-burning fossil fuels, industry emissions, vehicular exhaust, and aerosol chlorofluorocarbons-that trap heat in the Earth's atmosphere and adversely impact air quality. Resulting higher global temperatures, extreme weather events, and rising sea levels lead to greater frequency of wildfires and floods, which, in turn, result in population displacements and threaten air and water quality, food and water security, economic and public health infrastructures, and societal safety. Climate change has direct and indirect impacts on human health and well-being across the globe, with disproportionate impact on vulnerable populations including women, pregnant persons, the developing fetus, children, older adults, indigenous peoples, persons with disabilities, preexisting and/or chronic medical conditions, and low income and communities of color. As consequences of climate change, global mortality and noncommunicable diseases are mounting because of lack of progress to reverse current trends. Climate change effects on reproductive processes and outcomes have received less attention globally, despite huge consequences for human development, fertility, and pregnancy outcomes. This review provides evidence for direct and indirect effects of climate change on human health with a focus on reproductive processes and outcomes based on experimental models and epidemiologic data, and strategies to mitigate harms. The goal is to increase awareness about climate effects on reproductive health among clinicians, researchers, the public, and policymakers, and to engage all stakeholders to change the current trajectory of harm.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":"908-921"},"PeriodicalIF":23.9,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12640714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jiawen Dong, Kaitlyn M J H Dennis, Radha Venkatakrishnan, Leanne Hodson, Jeremy W Tomlinson
{"title":"The Impact of Estrogen Deficiency on Liver Metabolism: Implications for Hormone Replacement Therapy.","authors":"Jiawen Dong, Kaitlyn M J H Dennis, Radha Venkatakrishnan, Leanne Hodson, Jeremy W Tomlinson","doi":"10.1210/endrev/bnaf018","DOIUrl":"10.1210/endrev/bnaf018","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD; previously nonalcoholic fatty liver disease) is the most common chronic liver condition globally. It affects 1 in 3 individuals and is associated with increased liver and cardiovascular mortality. MASLD is a sexually dimorphic condition, and in women the prevalence and severity of MASLD rises significantly following menopause. Preclinical data shows that lack of estrogen promotes multisystem metabolic dysfunction that is characteristic of MASLD. This not only includes hepatic lipid accumulation, insulin resistance, and fibrosis but also extra-hepatic metabolic processes in adipose and skeletal muscle. There are currently no available MASLD treatments tailored to women. The uptake of estrogen-based menopausal hormone replacement therapy (HRT) has seen a dramatic increase in recent years. Despite the changing attitudes toward HRT and the strong evidence base implicating estrogen deficiency in the development of MASLD, the impact of HRT on MASLD in postmenopausal women is poorly studied. In this review, we discuss the burden of MASLD in women, the effect of estrogen deficiency on the processes that drive MASLD development and progression, and the potential sex-specific therapeutic strategies that may prevent or limit MASLD development after menopause.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":"790-809"},"PeriodicalIF":23.9,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12640711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yun Yang,Shanshan Zhang,Xiao Fang,Tengqi Shao,Xuan Shao,Yan-Ling Wang
{"title":"Placental Steroid Hormones in Preeclampsia: Multilayered Regulation of Endocrine Pathogenesis.","authors":"Yun Yang,Shanshan Zhang,Xiao Fang,Tengqi Shao,Xuan Shao,Yan-Ling Wang","doi":"10.1210/endrev/bnaf039","DOIUrl":"https://doi.org/10.1210/endrev/bnaf039","url":null,"abstract":"The human placenta serves as the predominant endocrine organ throughout pregnancy, assuming a central role in preserving endocrine homeostasis, facilitating maternal physiological adaptation, and safeguarding fetal well-being. Preeclampsia (PE), a multifaceted and systemic gestational complication, stands a primary contributor to maternal and perinatal morbidity and mortality. Defective placental development has been extensively acknowledged as the fundamental pathological foundation underlying this condition. Accumulating evidence has unveiled a disruption in the balance of steroid hormone production within placentas affected by early-onset PE (E-PE). Considerable endeavors have been undertaken to decipher the endocrine mechanisms driving E-PE. Recent investigations have illuminated a complex, multi-tiered regulatory system that governs placental steroidogenesis, encompassing epigenetic controls such as microRNAs (miRNAs) activity and metabolic flux-conjugated histone acetylation, post-translational modifications including O-linked β-N-acetylglucosamine (O-GlcNAc), as well as intricate endocrine feedback loops among steroids and other signaling molecules like melatonin. Notably, a growing body of evidence robustly supports a causal link between elevated placental testosterone (T0) synthesis and the onset of PE. Nevertheless, comprehensive studies exploring the endocrine pathophysiology of PE remain essential to illuminate novel therapeutic avenues for mitigating this adverse pregnancy outcome.","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":"128 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145433989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}