Current Opinion in Nephrology and Hypertension最新文献_第2页

Fibroblast growth factor 23 as a risk factor for incident diabetes. 成纤维细胞生长因子23作为发生糖尿病的危险因素。

IF 2.2 3区医学

Current Opinion in Nephrology and Hypertension Pub Date : 2025-07-01 Epub Date: 2025-04-15 DOI: 10.1097/MNH.0000000000001078

Martin H de Borst

{"title":"Fibroblast growth factor 23 as a risk factor for incident diabetes.","authors":"Martin H de Borst","doi":"10.1097/MNH.0000000000001078","DOIUrl":"10.1097/MNH.0000000000001078","url":null,"abstract":"Purpose of review: Diabetes is a major global health concern, affecting millions and increasing morbidity and mortality. Recent research highlights fibroblast growth factor 23 (FGF23) as a potential contributor to type 2 diabetes and its cardiovascular complications. This review explores the role of FGF23 in metabolic and cardiovascular dysfunction and discusses possible therapeutic interventions.Recent findings: Deregulated FGF23 is linked to insulin resistance, pancreatic β-cell dysfunction, and systemic inflammation. Studies suggest FGF23 influences glucose metabolism via insulin signaling, oxidative stress, and inflammation. Epidemiological data indicate that elevated FGF23 levels are associated with an increased risk of type 2 diabetes and posttransplant diabetes, independent of traditional risk factors. Higher FGF23 levels have also been linked with an increased cardiovascular risk in patients with diabetes, even without chronic kidney disease.Summary: FGF23 is emerging as a key factor in the cardiovascular-kidney-metabolic syndrome, connecting diabetes and cardiovascular disease. While studies suggest consistent associations, causal mechanisms remain unclear. No therapies specifically target FGF23 to lower diabetes risk, but fibroblast growth factor receptor 4 (FGFR4) inhibitors show promise. Future research should examine the role of FGF23 in individuals with normal kidney function and explore whether modifying its levels could reduce diabetes and cardiovascular risk.","PeriodicalId":10960,"journal":{"name":"Current Opinion in Nephrology and Hypertension","volume":" ","pages":"284-290"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12144538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of calprotectin in vascular calcification. 钙保护蛋白在血管钙化中的作用。

IF 2.2 3区医学

Current Opinion in Nephrology and Hypertension Pub Date : 2025-07-01 Epub Date: 2025-03-29 DOI: 10.1097/MNH.0000000000001075

Ana Amaya-Garrido, Julie Klein

{"title":"The role of calprotectin in vascular calcification.","authors":"Ana Amaya-Garrido, Julie Klein","doi":"10.1097/MNH.0000000000001075","DOIUrl":"10.1097/MNH.0000000000001075","url":null,"abstract":"Purpose of review: Vascular calcification significantly contributes to cardiovascular morbidity and mortality, particularly in high-risk populations like chronic kidney disease (CKD) patients. Calprotectin, a heterodimeric protein with pro-inflammatory and pro-calcific properties, has emerged as a key molecule in vascular pathology. This review highlights the mechanisms linking calprotectin to vascular calcification, its clinical relevance, and its potential as a therapeutic target.Recent findings: Vascular calcification is an active, cell-mediated process involving vascular smooth muscle cell (VSMC) dysfunction, inflammation, matrix remodeling, and cellular senescence. Calprotectin is strongly associated with cardiovascular disease and vascular calcification, particularly in CKD. Mechanistic studies reveal that calprotectin promotes calcification through the activation of RAGE and TLR4 signaling pathways, driving inflammatory cascades. Preclinical studies demonstrate that pharmacological inhibition of calprotectin attenuates vascular calcification in animal models, supporting its potential as a therapeutic target.Summary: Calprotectin is emerging as a promising biomarker and therapeutic target in vascular calcification, particularly in CKD and aging-related vascular diseases. However, further studies are required to clarify its mechanisms and assess the long-term efficacy and safety of calprotectin-targeted therapies. A deeper understanding of calprotectin's multifaceted role could pave the way for innovative therapeutic strategies targeting both inflammation and mineralization in calcification-related vascular diseases.","PeriodicalId":10960,"journal":{"name":"Current Opinion in Nephrology and Hypertension","volume":" ","pages":"276-283"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of osteopontin in chronic kidney disease-mineral bone disorder. 骨桥蛋白在慢性肾病-矿物质骨紊乱中的作用。

IF 2.2 3区医学

Current Opinion in Nephrology and Hypertension Pub Date : 2025-07-01 Epub Date: 2025-04-01 DOI: 10.1097/MNH.0000000000001074

Eduardo J Duque, Cecilia Giachelli, Rosa M A Moysés

{"title":"The role of osteopontin in chronic kidney disease-mineral bone disorder.","authors":"Eduardo J Duque, Cecilia Giachelli, Rosa M A Moysés","doi":"10.1097/MNH.0000000000001074","DOIUrl":"10.1097/MNH.0000000000001074","url":null,"abstract":"Purpose of review: Chronic kidney disease-mineral bone disorder (CKD-MBD) is associated with several adverse outcomes, including bone fragility and sarcopenia. Identification of new agents mitigating systemic damage related to uremia is critical and needed to unveil pathways implicated in CKD-MBD.Recent findings: Osteopontin (OPN) is involved in different physiological and pathological processes and works as a bridge connecting several systems. It may serve as a biomarker for many diseases, including human cancers, neurodegenerative disorders and autoimmune diseases. OPN has been implicated in disturbances of bone mineralization and remodeling, and has an interplay with parathyroid hormone and FGF23 in experimental models. In patients with CKD and severe hyperparathyroidism, OPN expression in muscle tissue has been linked to worse functionality and local inflammation, which is partially reverted after parathyroidectomy.Summary: Future studies could confirm the role of OPN as a biomarker in nephrology. Greater understanding of its role in CKD-MBD will help us define a better therapeutic strategy in patients with CKD.","PeriodicalId":10960,"journal":{"name":"Current Opinion in Nephrology and Hypertension","volume":" ","pages":"291-296"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143751562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of aging on chronic kidney disease mineral and bone disorder. 衰老对慢性肾脏疾病、矿物质和骨骼紊乱的影响。

IF 2.2 3区医学

Current Opinion in Nephrology and Hypertension Pub Date : 2025-07-01 Epub Date: 2025-05-02 DOI: 10.1097/MNH.0000000000001084

Washington A Freire-Filho, Maria Aparecida Dalboni, Rosilene M Elias

{"title":"Effects of aging on chronic kidney disease mineral and bone disorder.","authors":"Washington A Freire-Filho, Maria Aparecida Dalboni, Rosilene M Elias","doi":"10.1097/MNH.0000000000001084","DOIUrl":"10.1097/MNH.0000000000001084","url":null,"abstract":"Purpose of review: Aging and chronic kidney disease mineral and bone disorder (CKD-MBD) interact to worsen bone health, vascular calcification, and frailty in older patients. The altered FGF23-Klotho axis and disrupted mineral homeostasis emphasize the need for early interventions to mitigate fractures and cardiovascular complications in this vulnerable population. This review provides an updated overview of the current knowledge on CKD-MBD in older patients.Recent findings: CKD-MBD exacerbates bone fragility and vascular calcification in older populations. Early vascular aging and cognitive decline are associated with increased mortality. Disruptions in calcium, phosphate, and vitamin D homeostasis accelerate bone loss and fracture risk, whereas secondary hyperparathyroidism worsens cardiovascular outcomes. Additionally, polypharmacy, sarcopenia, and cognitive impairment further intensified the clinical burden in aging CKD patients.Summary: Aging potentially worsens CKD-MBD, vascular calcification, and cardiovascular disease in older patients. This growing field offers promising opportunities for further research to enhance understanding, improve bone health outcomes, and reduce fracture risk.","PeriodicalId":10960,"journal":{"name":"Current Opinion in Nephrology and Hypertension","volume":" ","pages":"297-303"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Chronic kidney disease and sex dimorphism. 慢性肾脏疾病和两性异形。

IF 2.2 3区医学

Current Opinion in Nephrology and Hypertension Pub Date : 2025-07-01 Epub Date: 2025-05-14 DOI: 10.1097/MNH.0000000000001093

Sarah Abu Kar, Raymond C Harris

{"title":"Chronic kidney disease and sex dimorphism.","authors":"Sarah Abu Kar, Raymond C Harris","doi":"10.1097/MNH.0000000000001093","DOIUrl":"10.1097/MNH.0000000000001093","url":null,"abstract":"Purpose of review: This review highlights studies published in the last 18 months focusing on sex dimorphism in clinical and preclinical areas related to chronic kidney disease (CKD).Recent findings: Hypertension, cardiorenal disease, hormone exposure, heat stress and dietary intake are all risk factors with sexually dimorphic effects thus contributing differentially to the development of chronic kidney disease. In CKD, GFR decline and cardiovascular mortality are more pronounced in males. Females have higher STEMI related in hospital mortality. When on dialysis, females have higher cardiovascular events rate. Males develop anemia and hyperparathyroidism earlier. Hyperphosphatemia is more prevalent in males. Vitamin D deficiency is associated with CKD in males only. Males are more likely to develop severe sarcopenia. The renoprotective effects of estrogen or estrogen agonists are mediated in part through GPER. ET-1 dual antagonism offset the action of GPER. ET-1 dual antagonism abolished the sex differences in acclimation to high salt. Sodium transport and oxygen consumption across the different renal segments is sexually dimorphic. Sexually dimorphic gene expression is mostly seen in the proximal tubules and is under androgen control.Summary: The above findings emphasize the need to systematically include female models in preclinical and clinical research which will improve clinical management and allow for development and implementation of precision medicine tailored to sex.","PeriodicalId":10960,"journal":{"name":"Current Opinion in Nephrology and Hypertension","volume":" ","pages":"314-321"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Updates on renal phosphate transport. 肾磷转运的最新进展。

IF 2.2 3区医学

Current Opinion in Nephrology and Hypertension Pub Date : 2025-07-01 Epub Date: 2025-05-13 DOI: 10.1097/MNH.0000000000001090

Carsten Alexande Wagner, Daniela Egli-Spichtig, Isabel Rubio-Aliaga

{"title":"Updates on renal phosphate transport.","authors":"Carsten Alexande Wagner, Daniela Egli-Spichtig, Isabel Rubio-Aliaga","doi":"10.1097/MNH.0000000000001090","DOIUrl":"10.1097/MNH.0000000000001090","url":null,"abstract":"Purpose of review: The kidneys control systemic phosphate balance by regulating phosphate transporters mediating the reabsorption of inorganic phosphate (Pi). At least three different Na + -driven Pi cotransporters are located in the brush border membrane (BBM) of proximal tubule cells, NaPi-IIa (SLC34A1), NaPi-IIc (SLC34A3) and PiT-2 (SLC20A2). This review will discuss novel aspects of their regulation, pharmacology, and genetics.Recent findings: Renal NaPi transporters are not only acutely regulated by the phosphaturic hormones parathyroid hormone (PTH) and Fibroblast Growth Factor 23 (FGF23) but possibly also by further mechanisms. A role of inositol hexakisphosphate (IP6) kinases has been found and their deletion from kidneys causes hypophosphatemia, hyperphosphaturia, and bone demineralization. Inhibitors of NaPis elicit phosphaturia and may reduce levels of PTH and FGF23 in chronic kidney disease (CKD) models. The relevance of renal NaPi transporters is highlighted by loss-of-function mutations in SLC34 transporters and analysis of patients provides new insights into diseases caused by variants. Major manifestations include nephrocalcinosis and -lithiasis, rickets, and variants may predispose to an accelerated decline in kidney function.Summary: Renal Pi transporters are regulated, may provide novel drug targets for prevention or treatment of hyperphosphatemia, and contribute to the genetic risk to develop kidney stones and CKD.","PeriodicalId":10960,"journal":{"name":"Current Opinion in Nephrology and Hypertension","volume":" ","pages":"269-275"},"PeriodicalIF":2.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12144537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143972792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transport and thiazide-inhibition mechanisms of the Na-Cl cotransporter: a structural perspective. Na-Cl共转运体的转运和噻嗪类药物抑制机制：结构视角。

IF 2.2 3区医学

Current Opinion in Nephrology and Hypertension Pub Date : 2025-06-27 DOI: 10.1097/MNH.0000000000001099

Chien-Ling Lee, Liang Feng

{"title":"Transport and thiazide-inhibition mechanisms of the Na-Cl cotransporter: a structural perspective.","authors":"Chien-Ling Lee, Liang Feng","doi":"10.1097/MNH.0000000000001099","DOIUrl":"10.1097/MNH.0000000000001099","url":null,"abstract":"Purpose of review: The structures of the human sodium-chloride cotransporter (hNCC) and its complex with thiazide diuretics have been determined recently. This review summarizes key structural insights into NCC's transport and inhibition mechanisms.Recent findings: Recent studies revealed the structures of hNCC and its complex with thiazide diuretics, in inward-facing and outward-facing conformations, respectively. The structures of hNCC in two major conformational states provided important insights into the transport and regulatory mechanisms. Thiazide-bound hNCC structures illuminated the molecular mechanisms of thiazide-mediated NCC inhibition and explained the structure-activity relationship of thiazide diuretics.Summary: Structures of hNCC provide mechanistic insights into molecular mechanisms of loss-of-function NCC variants that cause Gitelman syndrome. The thiazide-bound hNCC structures provide a blueprint for further optimizing thiazide diuretics to reduce side effects. The novel interdomain interaction-mediated hNCC regulatory mechanisms revealed by structural studies lay the foundation for developing next-generation NCC modulators and NCC-rescuing therapeutics for treating NCC dysfunction.","PeriodicalId":10960,"journal":{"name":"Current Opinion in Nephrology and Hypertension","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505068","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A current update of the development of Chimeric Antigen Receptor T-cell therapy and kidney disease. 嵌合抗原受体t细胞治疗和肾脏疾病的最新进展。

IF 2.2 3区医学

Current Opinion in Nephrology and Hypertension Pub Date : 2025-06-24 DOI: 10.1097/MNH.0000000000001096

Juan León-Román, Alexandra Esteves, Gloria Iacoboni, María José Soler

{"title":"A current update of the development of Chimeric Antigen Receptor T-cell therapy and kidney disease.","authors":"Juan León-Román, Alexandra Esteves, Gloria Iacoboni, María José Soler","doi":"10.1097/MNH.0000000000001096","DOIUrl":"https://doi.org/10.1097/MNH.0000000000001096","url":null,"abstract":"Purpose of review: Chimeric antigen receptor (CAR) T-cell therapy has marked a historic milestone for its remission rates in relapsed/refractory hematological neoplasms. Despite favorable efficacy outcomes, CAR T-cells are associated with potentially severe early and late complications, such as cytokine release syndrome (CRS), neurotoxicity, acute kidney injury (AKI), cytopenias and infections.Recent findings: AKI is a common complication that normally manifests during the first week following infusion and typically shows recovery within the first month. The risk factors for AKI development include a prior history of chronic kidney disease (CKD), development of CRS or neurotoxicity, antibiotic therapy and the use of intravenous contrast, amongst others.Summary: AKI a frequent but mild complication, with fast recovery. Future multicentric prospective studies are required to investigate the pathophysiology of AKI following CAR T-cell therapy and the potential preventive treatments. Furthermore, the impact of AKI secondary to CAR T-cell treatment in patients with prior CKD has not been analyzed in long-term follow-up studies.","PeriodicalId":10960,"journal":{"name":"Current Opinion in Nephrology and Hypertension","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144474199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Moving beyond the syndrome: how can acute kidney injury phenotypes help? 超越症候群：急性肾损伤表型如何起作用？

IF 2.2 3区医学

Current Opinion in Nephrology and Hypertension Pub Date : 2025-06-13 DOI: 10.1097/MNH.0000000000001098

Jennifer Scott, Emily J See, Yvelynne P Kelly

{"title":"Moving beyond the syndrome: how can acute kidney injury phenotypes help?","authors":"Jennifer Scott, Emily J See, Yvelynne P Kelly","doi":"10.1097/MNH.0000000000001098","DOIUrl":"10.1097/MNH.0000000000001098","url":null,"abstract":"Purpose of review: The purpose of this review is to describe recent and important updates in acute kidney injury (AKI) phenotyping that help us to move beyond the clinical syndrome of AKI.Recent findings: Recent studies reinforce the utility of damage biomarker positivity in AKI classification and have found that biomarker positivity (specifically NGAL) adds prognostic information regardless of classification of the AKI according to RIFLE or KDIGO criteria, and regardless of cut-off selection methodology. Novel methodologies for identifying AKI phenotypes and subphenotypes are currently being developed and integrated subclassification approaches e.g. combining biomarker and transcriptomic approaches, have been found to be more informative than using a single approach alone to identify AKI phenotypes. Consortiums have developed in partnership between academia and industry to identify consensus endotypes for critically ill adults and children.Summary: There are prognostic and treatment benefits to AKI phenotyping and subphenotyping which allow us to provide a customized approach to AKI care. Challenges currently exist to implementation of AKI phenotyping at the bedside but ongoing projects are already seeking solutions for feasible bedside identification of subphenotypes using machine-learning or point-of-care biomarker assays. Future research in this area will focus on the ability to recognize and link endotypes, subphenotypes and phenotypes in AKI.","PeriodicalId":10960,"journal":{"name":"Current Opinion in Nephrology and Hypertension","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Novel insights in the regulation of intercalated cell differentiation. 插层细胞分化调控的新见解。

IF 2.2 3区医学

Current Opinion in Nephrology and Hypertension Pub Date : 2025-06-05 DOI: 10.1097/MNH.0000000000001095

Yu Feng, Yanmiao Qi, Xiangjian Zheng

{"title":"Novel insights in the regulation of intercalated cell differentiation.","authors":"Yu Feng, Yanmiao Qi, Xiangjian Zheng","doi":"10.1097/MNH.0000000000001095","DOIUrl":"https://doi.org/10.1097/MNH.0000000000001095","url":null,"abstract":"Purpose of review: Kidney intercalated cells play critical roles in regulating body acid-base balance. We recently discovered Foxp1 and two downstream transcriptional factors Dmrt2 and Hmx2 are essential for intercalated cell differentiation. This review incorporates these findings with previous reports to add insights to the molecular regulation of intercalated cell differentiation.Recent findings: We reviewed the current understanding of intercalated cell differentiation and plasticity, and the contribution of single-cell sequencing to point to the existence of transitional cells during principal cell and intercalated cell differentiation or trans-differentiation. For molecular regulation of cell differentiation, we discuss how Notch and Foxi1 regulate principal cell/intercalated cell switch and intercalated cell differentiation, and the new finding of Foxp1 and downstream transcriptional factors in intercalated cell subtype specification.Summary: The differentiation and balance of principal cell and intercalated cell subtypes are the foundation for maintaining acid-base balance. A clear understanding of the cellular and molecular controls of these processes provides the basis for designing intervention approaches for metabolism acidosis or alkalosis and other related diseases.","PeriodicalId":10960,"journal":{"name":"Current Opinion in Nephrology and Hypertension","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0