Shuai Guo, Hong-Min Luo, Ling-Ling Wang, Xin-Ai Huo, Yan-Qing Chi
{"title":"The interplay between endothelial cell dysfunction and podocyte injury in diabetic nephropathy: a comprehensive review of current evidence.","authors":"Shuai Guo, Hong-Min Luo, Ling-Ling Wang, Xin-Ai Huo, Yan-Qing Chi","doi":"10.62347/QQMX6273","DOIUrl":null,"url":null,"abstract":"<p><p>Diabetic nephropathy (DN) remains the leading cause of end-stage renal disease globally. Emerging evidence highlights the bidirectional crosstalk between glomerular endothelial cell (GEC) dysfunction and podocyte injury as a key driver of DN progression. This review synthesizes current understanding of the molecular mechanisms, clinical correlations, and therapeutic strategies targeting this interplay. Mechanistically, hyperglycemia-induced oxidative stress, dysregulated angiogenesis, and aberrant extracellular vesicle (EV)-mediated signaling contribute to a self-perpetuating cycle of glomerular injury. Clinically, biomarkers of endothelial-podocyte axis disruption predict disease progression and therapeutic response. Novel therapies, including endothelin receptor antagonists, sodium-glucose cotransporter 2 (SGLT2) inhibitors, and mesenchymal stem cell derived EVs, show promise for restoring glomerular filtration barrier (GFB) integrity. This review integrates multi-omics insights to propose a unified model of DN pathogenesis and precision medicine approaches.</p>","PeriodicalId":7731,"journal":{"name":"American journal of translational research","volume":"17 8","pages":"5862-5870"},"PeriodicalIF":1.6000,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12432703/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of translational research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.62347/QQMX6273","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
Abstract
Diabetic nephropathy (DN) remains the leading cause of end-stage renal disease globally. Emerging evidence highlights the bidirectional crosstalk between glomerular endothelial cell (GEC) dysfunction and podocyte injury as a key driver of DN progression. This review synthesizes current understanding of the molecular mechanisms, clinical correlations, and therapeutic strategies targeting this interplay. Mechanistically, hyperglycemia-induced oxidative stress, dysregulated angiogenesis, and aberrant extracellular vesicle (EV)-mediated signaling contribute to a self-perpetuating cycle of glomerular injury. Clinically, biomarkers of endothelial-podocyte axis disruption predict disease progression and therapeutic response. Novel therapies, including endothelin receptor antagonists, sodium-glucose cotransporter 2 (SGLT2) inhibitors, and mesenchymal stem cell derived EVs, show promise for restoring glomerular filtration barrier (GFB) integrity. This review integrates multi-omics insights to propose a unified model of DN pathogenesis and precision medicine approaches.
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