ReviewFrontiers in cell and developmental biology2025
Podocytes in health and glomerular disease.
Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The trial behind it
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Who cites it
22 citing papers in PubMed.
- MiR-423-5p inhibition alleviates podocyte apoptosis in membranous nephropathy by targeting WT1/β-catenin axis.International urology and nephrology · 2026Article
- Beyond cytoskeletal regulation: Rho-associated, coiled-coil-containing protein kinase 2 in kidney inflammation and fibrosis.Histology and histopathology · 2026Review
- WTAP Deficiency Promotes Podocyte PANoptosis and FSGS via SPP1 Signaling.Circulation research · 2026Article
- The ELAVL1-PLAUR-suPAR Axis Exacerbates Diabetic Nephropathy by Promoting Podocyte Injury and Inflammation.Journal of diabetes · 2026Article
- Single-cell and high-resolution spatial profiling of podocytopathies reveals core mechanisms of podocyte injury.Science advances · 2026Article
- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Inhibiting the P2X7R-NLRP3 inflammasome pathway regulates CXCL16 to alleviate podocyte injury in mice with adriamycin nephropathy.Scientific reports · 2026Article
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- Molecular Mechanisms and Clinical Evidence Supporting the Four Pillars of Therapy in Diabetic Kidney Disease: Emerging Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Mitochondrial Dynamics in Diabetic Kidney Disease: Underlying Mechanisms and Novel Therapeutics.International journal of molecular sciences · 2026Review
- Piezo1-Mediated Mechanotransduction: Orchestrating the Dynamic Response of Podocytes and Parietal Epithelial Cells to Mechanical Stress.Acta physiologica (Oxford, England) · 2026Review
- Exploring the mechanism by which modified huangqi chifeng decoction protects podocytes via Arid5a-mediated transcriptional regulation of the AIM2 pyroptosis signaling axis.Frontiers in immunology · 2026Article
- Emerging roles of cannabinoid pathways in renal injury and repair.Frontiers in pharmacology · 2026Review
- DJ-1 alleviates high glucose-induced podocyte injury via activating ERK1/2 signaling.PloS one · 2026Article
- SSB deficiency-induced R-loop accumulation triggers podocyte inflammation in DKD.Frontiers in immunology · 2026Article
- Yiqi Huoxue Yangyin Decoction attenuates diabetic nephropathy inFrontiers in pharmacology · 2026Article
- Yiqi Huoxue Yangyin Decoction Ameliorates Diabetic Nephropathy by Targeting AMPK/mTOR-Mediated Autophagy: A Network Pharmacology-Guided in vivo and in vitro Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Longitudinal trajectories of urinary albumin-to-creatinine ratio and risk of proteinuria among Chinese patients with type 2 diabetes: a single-center retrospective cohort study.Frontiers in endocrinology · 2026Article
- Comprehensive snRNA-Seq Datasets of Human and Mouse Podocytopathy Integrated with GWAS of Microalbuminuria.Scientific data · 2025Article
- Qing-Re-Xiao-Zheng-yi-qi formula protects renal function by stabilizing lysosomal membranes and inhibiting NLRP3-inflammasome-mediated pyroptosis in diabetic kidney disease.Annals of medicine · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocytes are highly specialized, terminally differentiated cells in the glomerulus of the kidney and these cells play a central role in blood filtration. In this review, we comprehensively describe the cell biology of podocytes under healthy conditions and in glomerular disorders wherein podocyte injury is a major pathological mechanism. First, the molecular mechanisms that maintain podocyte actin cytoskeleton structure, permanent cell cycle exit, and metabolism under healthy conditions are described. Secondly, the mechanisms of podocyte injury, including genetic alterations and external insults that ultimately disrupt podocyte actin cytoskeleton dynamics or interrupt podocyte quiescence and mitochondrial metabolism are discussed. This understanding forms the basis of described potential therapeutic agents that act by modulating dysregulated podocyte cytoskeleton organization, prevent or reverse cell cycle re-entry, and re-establish normal mitochondrial energy production. Lastly, the application of modern techniques such as single cell RNA sequencing, super resolution microscopy, atomic force microscopy, and glomerular organoids is improving the resolution of mechanistic podocytopathy knowledge. Taken together, our review provides critical insights into the cellular and molecular mechanisms leading to podocyte loss, necessary for the advancement of therapeutic development in glomerular diseases.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.