Endocrinology and metabolism (Seoul, Korea)最新文献

{"title":"Consensus on the Diagnosis of Cushing's Disease: A Collaborative Statement from the Korean Endocrine Society and Japan Endocrine Society.","authors":"Jeongmin Lee, Hidenori Fukuoka, Seung Shin Park, A Ram Hong, Jung Hee Kim, Sang Ouk Chin, Han-Sang Baek, Dong-Jun Lim, Kazunori Kageyama, Mitsuru Nishiyama, Shigeyuki Tahara, Kenichi Oyama, Akira Sugawara, Miho Yamashita, Naoko Inoshita, Hiroshi Arima, Byung-Joon Kim, Yoon-Sok Chung, Soon Jib Yoo, Michio Otsuki, Mi-Kyung Kim","doi":"10.3803/EnM.2025.2707","DOIUrl":"10.3803/EnM.2025.2707","url":null,"abstract":"<p><p>Cushing's disease (CD) is a rare but serious endocrine disorder caused by excessive cortisol secretion due to adrenocorticotropic hormone-secreting pituitary tumors. Despite recent developments in diagnostic criteria and treatment options, CD remains associated with substantial comorbidities and mortality. Early and accurate diagnosis is thus essential. Both the Korean Endocrine Society (KES) and Japan Endocrine Society (JES) guidelines are intended to standardize diagnostic approaches to CD, and they share common principles; however, notable differences exist, particularly in biochemical testing thresholds and imaging recommendations. This consensus statement integrates clinical evidence and expert practice from both the KES and JES to establish harmonized recommendations for biochemical evaluation, imaging, and differential testing. This unified framework is intended to enhance diagnostic precision and improve clinical outcomes across East Asian populations.</p>","PeriodicalId":520607,"journal":{"name":"Endocrinology and metabolism (Seoul, Korea)","volume":" ","pages":"1-13"},"PeriodicalIF":4.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New Sparks and Spots: Molecular Imaging with Positron Emission Tomography Will Change Management of Cushing's Disease.","authors":"Martin Reincke, Tugce Apaydin, Mariam Kakashvili, Nathalie L Albert, Jun Thorsteinsdottir, Júnia R O L Schweizer, Marily Theodoropoulou, Katharina Schilbach, Friederike Völter","doi":"10.3803/EnM.2025.2728","DOIUrl":"10.3803/EnM.2025.2728","url":null,"abstract":"<p><p>Cushing's disease is caused by corticotroph tumors of the pituitary gland, resulting in adrenocorticotropic hormone hypersecretion and cortisol excess. The majority of the tumors are microadenomas. Magnetic resonance imaging (MRI) imaging is able to detect up to 70% of the corticotroph tumors. In the remaining patients, no tumor is detectable on MRI or there are equivocal changes without a clear demarcation of a tumor. Hence, the cure rates following transsphenoidal pituitary surgery are far from being satisfactory, with around 60% to 90% short-term remission in expert centers. Positron emission tomography (PET) has recently emerged as a potent method for the localization of small corticotroph adenomas and corticotroph adenomas without demarcation on the MRI. This review analyzes the radiopharmaceuticals most commonly used in evaluating pituitary disorders and explores the potential utilization of new PET tracers for personalized management of patients with Cushing's disease. Especially 11C-methionine and 18F-fluorethyltyrosine PET have recently been reported to be highly sensitive methods to detect MRI-undetectable corticotropinomas in 80% to 100% of patients. If confirmed in randomized controlled trials, PET imaging could be a major break-through towards targeted, individualized surgical therapy.</p>","PeriodicalId":520607,"journal":{"name":"Endocrinology and metabolism (Seoul, Korea)","volume":" ","pages":"49-56"},"PeriodicalIF":4.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146115425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced Sphingosine-1-Phosphate Levels Exacerbate Type 2 Diabetes Mellitus and Associated Complications in a High-Fat Diet Mouse Model.","authors":"Shih-Chang Hsu, Ching-Lu Chen, Chung Te Liu, Hung-Chieh Lo, Ying-Kuo Liu, Pei-Song Gao, Shau-Ku Huang, Chin-Wang Hsu","doi":"10.3803/EnM.2025.2360","DOIUrl":"10.3803/EnM.2025.2360","url":null,"abstract":"<p><strong>Backgruound: </strong>Type 2 diabetes mellitus (T2DM) is increasingly prevalent and frequently associated with obesity, insulin resistance, nonalcoholic fatty liver disease, and chronic kidney disease. Emerging evidence suggests sphingosine-1-phosphate (S1P), a bioactive sphingolipid, plays a significant role in the pathogenesis of T2DM. This study aimed to investigate how reduced S1P levels impact T2DM development.</p><p><strong>Methods: </strong>S1P lyase knock-in (S1PLC317A KI) mice, characterized by reduced S1P levels due to impaired S1P degradation, were compared with wild-type (WT) mice. Both groups were fed a high-fat diet (HFD) to induce T2DM. Parameters including body weight, insulin resistance, blood glucose levels, hepatic fat accumulation, and kidney pathology were evaluated. Next-generation sequencing was employed to identify differentially expressed genes.</p><p><strong>Results: </strong>S1PLC317A KI mice exhibited greater body weight, more pronounced insulin resistance, and higher blood glucose levels compared to WT mice on an HFD. Increased hepatic fat deposition and worsened diabetic kidney disease were also observed in KI mice. Sequencing analysis identified 4,656 differentially expressed genes, notably enriched in mitochondrial and bioenergetic pathways, including 133 diabetes-related genes.</p><p><strong>Conclusion: </strong>Reduced S1P levels exacerbate T2DM symptoms, indicating that therapeutic targeting of S1P pathways may offer promising strategies for treating T2DM and its related complications.</p>","PeriodicalId":520607,"journal":{"name":"Endocrinology and metabolism (Seoul, Korea)","volume":" ","pages":"108-120"},"PeriodicalIF":4.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963768/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144786415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Progranulin Deficiency on Inflammation and Fibrosis in the Kidneys and Liver of Diabetic Mice Fed a High-Fat Diet.","authors":"Hiroko Sakuma, Maki Murakoshi, Shinji Hagiwara, Terumi Shibata, Yusuke Suzuki, Tomohito Gohda","doi":"10.3803/EnM.2025.2339","DOIUrl":"10.3803/EnM.2025.2339","url":null,"abstract":"<p><strong>Backgruound: </strong>Progranulin (PGRN) is an important regulator of inflammation, insulin resistance, and autophagy. However, the effects of PGRN deficiency on these processes in the kidneys and liver in diabetes remain unclear. In addition, the differential effects of PGRN deficiency and sodium-glucose co-transporter-2 (SGLT2) inhibitors on these organs are unknown.</p><p><strong>Methods: </strong>Three diabetic mouse models were used: high-fat diet and nicotinamide/streptozotocin-induced diabetic wild-type (WT) and PGRN-knockout (KO) mice (WT-diabetes mellitus [DM] and KO-DM, respectively) and WT-DM mice treated with an SGLT2 inhibitor (tofogliflozin; WT-DM/Tofo).</p><p><strong>Results: </strong>Despite similar glycemic control in WT-DM/Tofo and KO-DM mice, expression of inflammation- and fibrosis-related genes in the kidneys was highest in WT-DM mice, lower in KO-DM mice, and lowest in WT-DM/Tofo mice. WT-DM/Tofo mice also showed increased anti-microtubule-associated protein 1A/1B-light chain 3B and decreased p62 protein levels compared with KO-DM mice. In contrast, hepatic mRNA levels related to inflammation and fibrosis were improved in both WT-DM/Tofo and KO-DM mice. Moreover, hepatic protein levels of peroxisome proliferator-activated receptor γ (PPARγ) were elevated in both groups compared with WT-DM mice, while those of PPARα were increased in WT-DM/Tofo mice compared with both WT-DM and KO-DM mice.</p><p><strong>Conclusion: </strong>Kidney inflammation and fibrosis were ameliorated in WT-DM/Tofo mice, but these improvements were limited by autophagy insufficiency in KO-DM mice. Additionally, both WT-DM/Tofo and KO-DM mice demonstrated improved liver inflammation and fibrosis; in the former, this was associated with enhanced fatty acid oxidation via PPARα activation, while in the latter, it appeared to result from improved insulin sensitivity and anti-inflammatory effects through PPARγ activation.</p>","PeriodicalId":520607,"journal":{"name":"Endocrinology and metabolism (Seoul, Korea)","volume":" ","pages":"138-151"},"PeriodicalIF":4.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963769/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145194385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nationwide Big Data Studies of Endocrine Diseases Using the Korean National Health Information Database: Research Trends and Standardization of Operational Definitions.","authors":"Sun Wook Cho, Jung Hee Kim, Kyoung Jin Kim, Beom-Jun Kim, Mee Kyoung Kim, Eun Jung Rhee","doi":"10.3803/EnM.2026.2953","DOIUrl":"10.3803/EnM.2026.2953","url":null,"abstract":"<p><p>The Korean National Health Information Database (NHID) is a large-scale dataset created through linkage of National Health Insurance claims with nationwide health screening records. Because it is released in a cohort-based format, the NHID enables longitudinal follow-up and allows investigation of rare endocrine conditions with low population prevalence. Mortality data, including both dates and causes of death, are additionally obtained through linkage with Statistics Korea. Over recent years, use of the NHID has expanded rapidly, establishing it as a major resource for epidemiological research in endocrinology. Nevertheless, because the database was originally developed for administrative and screening purposes rather than for research, investigators face several methodological limitations, particularly the need to construct and validate robust operational definitions of diseases. In this review, we describe the key features of the Korean NHID, summarize operational definitions of endocrine disorders that have been applied in prior research, and provide an overview of recent endocrine studies conducted using this database.</p>","PeriodicalId":520607,"journal":{"name":"Endocrinology and metabolism (Seoul, Korea)","volume":"41 1","pages":"86-104"},"PeriodicalIF":4.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147367857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LGALS3BP Induces Insulin Resistance via TLR2-IKKα/β Pathway-Mediated IRS1 Serine Phosphorylation.","authors":"Minjeong Sung, Dae-Hwan Kim, Eun-Gene Sun, Jun-Eul Hwang, Sang-Hee Cho, Ik-Joo Chung, Hyun-Jeong Shim, Woo Kyun Bae","doi":"10.3803/EnM.2025.2448","DOIUrl":"10.3803/EnM.2025.2448","url":null,"abstract":"<p><strong>Backgruound: </strong>Insulin resistance (IR) disrupts hepatic glucose and lipid metabolism, contributing to metabolic dysfunction-associated steatotic liver disease (MASLD) and progression to severe liver complications. Galectin-3-binding protein (LGALS3BP) is a secreted glycoprotein implicated in inflammation and metabolic disorders. Elevated LGALS3BP levels are associated with MASLD and type 2 diabetes (T2D), but its role in IR remains unclear.</p><p><strong>Methods: </strong>LGALS3BP-deficient models were used to investigate its role in IR and inflammation. Glucose metabolism and insulin signaling were assessed in high-fat diet (HFD)-fed mice. Hepatic cell lines were employed to evaluate the direct effects of LGALS3BP on insulin signaling and inflammation. Mechanistic insights were obtained through RNA sequencing, structural modeling, immunoprecipitation, and protein/gene expression analyses.</p><p><strong>Results: </strong>LGALS3BP deficiency improved insulin sensitivity in HFD-fed mice by enhancing glucose tolerance, lowering serum glucose and insulin, and increasing hepatic insulin signaling, without altering lipid accumulation. In vitro, LGALS3BP deficiency enhanced insulin signaling and suppressed gluconeogenesis, whereas recombinant LGALS3BP impaired insulin signaling and upregulated gluconeogenesis. RNA sequencing revealed activation of Toll-like receptor 2 (TLR2) and nuclear factor-kappa B (NF-κB) pathways by LGALS3BP. Immunoprecipitation confirmed a direct interaction between LGALS3BP and TLR2, leading to inhibitor kappa kinase (IKK)/NF-κB activation and increased insulin receptor substrate-1 (IRS1) serine phosphorylation, a key inhibitory modification in IR. Furthermore, LGALS3BP deficiency attenuated hepatic fibrosis under chronic HFD, accompanied by downregulated inflammatory signaling pathways.</p><p><strong>Conclusion: </strong>LGALS3BP contributes to IR through inflammatory responses, particularly via TLR2-IKKα/β signaling that regulates IRS1 serine phosphorylation. LGALS3BP deficiency improves insulin sensitivity and reduces inflammation, suggesting that targeting LGALS3BP may represent a potential therapeutic strategy for metabolic disorders such as T2D and MASLD.</p>","PeriodicalId":520607,"journal":{"name":"Endocrinology and metabolism (Seoul, Korea)","volume":" ","pages":"121-137"},"PeriodicalIF":4.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sarcopenia and Muscle Aging: Updated Insights into Molecular Mechanisms and Translational Therapeutics.","authors":"Thanh T Nguyen, Tam Dao, Ha Thu Nguyen, Jun-Hyeon Park, Seung-Jun Jeong, Sei Kim, Yunju Jo, Nhung T H Thieu, Jiangqi Zhao, Fuan Ding, Ying Yu, Vu Chi Dung, Karim Gariani, Beom-Jun Kim, Dongryeol Ryu","doi":"10.3803/EnM.2025.2656","DOIUrl":"10.3803/EnM.2025.2656","url":null,"abstract":"<p><p>Sarcopenia is a progressive, age-related condition characterized by the loss of skeletal muscle mass, strength, and function, which increases the risk of falls, frailty, and loss of independence. Despite growing recognition and its incorporation into geriatric assessments, there is still no approved pharmacological treatment. This review provides an updated overview of sarcopenia, encompassing diagnostic criteria, biological mechanisms, and emerging therapeutic strategies. Key molecular features include mitochondrial dysfunction, nicotinamide adenine dinucleotide (NAD⁺) decline, fiber-type alterations, and dysregulation of myokines. Recent singlecell and multi-omics studies have revealed the heterogeneity of muscle tissue and distinct cell-type-specific aging patterns. Therapeutic efforts are evolving beyond lifestyle interventions toward targeted approaches, including myostatin inhibitors, NAD⁺ boosters, senolytics, and microbiome modulators. However, clinical translation remains constrained by heterogeneity in trial design and the absence of standardized outcome measures. Future sarcopenia care will likely involve precision medicine guided by biomarkers and supported by digital monitoring tools. Progressing from molecular discovery to clinical application will be essential for preserving muscle health and function in aging populations.</p>","PeriodicalId":520607,"journal":{"name":"Endocrinology and metabolism (Seoul, Korea)","volume":" ","pages":"57-85"},"PeriodicalIF":4.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146169203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Comparative Evaluation of Three Time-to-Event Models Predicting 5-Year Osteoporosis Risk in Thyroid Cancer Survivors: A Nationwide Cohort Study.","authors":"Young Bin Cho, Kyoung Sik Park","doi":"10.3803/EnM.2025.2478","DOIUrl":"10.3803/EnM.2025.2478","url":null,"abstract":"<p><strong>Backgruound: </strong>Osteoporosis is a common complication among thyroid cancer survivors; however, predictive tools for this condition remain inadequate. This study aimed to develop time-to-event prediction models for assessing osteoporosis risk in thyroid cancer patients.</p><p><strong>Methods: </strong>Using the Korean National Health Insurance Service claims database, we identified 3,089 patients newly diagnosed with thyroid cancer between 2004 and 2014. Patients were randomly divided into training and test datasets in a 7:3 ratio. Three time-toevent models were constructed: random survival forest, Boruta-Cox proportional hazards, and least absolute shrinkage and selection operator (LASSO)-penalized Cox models, with feature selection and five-fold cross-validation. Model performance was evaluated using time-dependent area under the curve, Harrell's concordance index (C-index), and risk stratification analysis.</p><p><strong>Results: </strong>Among thyroid cancer survivors with a median follow-up of 4.2 years, the 5-year cumulative incidence of osteoporosis was 21%. The Boruta-Cox proportional hazards model achieved the highest C-index of 0.72 (95% confidence interval [CI], 0.68 to 0.75), outperforming the random survival forest (0.68 [95% CI, 0.65 to 0.71]) and the LASSO-penalized Cox model (0.64 [95% CI, 0.61 to 0.68]). Risk stratification analysis showed that all three models significantly distinguished between low- and high-risk groups (P<0.001).</p><p><strong>Conclusion: </strong>This study constructed well-performing prediction models for estimating osteoporosis risk in thyroid cancer survivors, demonstrating their utility in risk stratification.</p>","PeriodicalId":520607,"journal":{"name":"Endocrinology and metabolism (Seoul, Korea)","volume":" ","pages":"174-184"},"PeriodicalIF":4.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963770/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145663395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progranulin Deficiency Improves Metabolic Stress Yet Falls Short of Sodium-Glucose Cotransporter-2 Inhibition in Autophagy-Linked Renal Protection.","authors":"Seung-Soon Im","doi":"10.3803/EnM.2026.2948","DOIUrl":"10.3803/EnM.2026.2948","url":null,"abstract":"","PeriodicalId":520607,"journal":{"name":"Endocrinology and metabolism (Seoul, Korea)","volume":"41 1","pages":"105-107"},"PeriodicalIF":4.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147367886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Growth Hormone, Not Simply Just a Hormone for Growth.","authors":"Kevin C J Yuen, Jaime Guevara-Aguirre, John J Kopchick","doi":"10.3803/EnM.2025.2806","DOIUrl":"10.3803/EnM.2025.2806","url":null,"abstract":"<p><p>Since its discovery almost 100 years ago, growth hormone (GH) has been extensively studied to elucidate its structural characteristics, receptor interactions and its physiologic and non-physiologic effects. These actions include but are not limited to its effects on somatic growth, substrate metabolism, body composition, bone mineral density, cardiovascular system, and cognitive function. Contextually, recombinant human GH was approved for growth promotion in children and to enhance metabolic health in adult patients with GH deficiency (GHD), along with other clinical indications. Studies involving individuals and animal models exhibiting dysregulated GH levels, ranging from complete or partial GHD to GH excess, have unveiled a spectrum of several less evident GH actions. In this review, we exclude discussing the classic GH therapeutic applications but instead focus on the interplay between GH and glucose metabolism, fibrosis, and carcinogenesis that is observed with varying GH levels and action. We also discuss clinical data derived from studies in acromegaly and GHD patients (including individuals with congenital GH and insulin-like growth factor I [IGF-I] deficiencies), and attempt to integrate findings from cellular, animal and human studies with the aim of highlighting novel characteristics and underlying molecular pathways through which both GH and IGF-I exert their more subtle actions.</p>","PeriodicalId":520607,"journal":{"name":"Endocrinology and metabolism (Seoul, Korea)","volume":" ","pages":"34-48"},"PeriodicalIF":4.2,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146109671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}