Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (730 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Highly differentiated epithelial cells of the visceral layer of bowman capsule of the kidney. They are composed of a cell body with major cell surface extensions and secondary fingerlike extensions called pedicels. They enwrap the kidney glomerulus capillaries with their cell surface extensions forming a filtration structure. The pedicels of neighboring podocytes interdigitate with each other leaving between them filtration slits that are bridged by an extracellular structure impermeable to large macromolecules called the slit diaphragm, and provide the last barrier to protein loss in the kidney.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Podocyte; Epithelial Cells, Glomerular Visceral; Glomerular Visceral Epithelial Cells; Visceral Epithelial Cells, Glomerular.
Where it fits in the MeSH classification
- Broader topics
- Glomerular Filtration Barrier; Kidney Glomerulus; Epithelial Cells
Related concepts
- Bowman Capsule
- Kidney
- Cell Surface Extensions
- Kidney Glomerulus
Research landscape
PubMed indexes 6,484 records tagged with the MeSH heading “Podocytes” (counts retrieved 2026-10-31). 2,421 of them (37.3%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 3,304 records.
Reviews account for 896 records (13.8%) and meta-analyses for 4. Randomized controlled trials number 12 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 829 |
| 2010-2019 | 3,304 |
| 2020 onward | 2,421 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 896 | 13.8% |
| Meta-analyses | 4 | 0.1% |
| Randomized controlled trials | 12 | 0.2% |
Method: PubMed query "Podocytes"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Crosstalk among podocytes, glomerular endothelial cells and mesangial cells in diabetic kidney disease: an updated review | 2024 | Review article Design not recorded in structured metadata | 112 | cc by PMID 38374141 · DOI · PMC10875896 |
| Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy | 2023 | Review article Design not recorded in structured metadata | 42 | cc by PMID 38288116 · DOI · PMC10822972 |
| Renal Angptl4 is a key fibrogenic molecule in progressive diabetic kidney disease | 2024 | Research article Design not recorded in structured metadata | 37 | cc by PMID 39630889 · DOI · PMC11616692 |
| SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3 | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41316884 · DOI · PMC12904062 |
Crosstalk among podocytes, glomerular endothelial cells and mesangial cells in diabetic kidney disease: an updated review [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Diabetic kidney disease (DKD) is a long-term and serious complication of diabetes that affects millions of people worldwide.
- Closing excerpt
- In conclusion, this review provides a comprehensive and updated overview of the glomerular crosstalk in DKD and highlights its importance for the development of novel intervention approaches.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (200 words)
Diabetic kidney disease (DKD) is a long-term and serious complication of diabetes that affects millions of people worldwide. It is characterized by proteinuria, glomerular damage, and renal fibrosis, leading to end-stage renal disease, and the pathogenesis is complex and involves multiple cellular and molecular mechanisms. Among three kinds of intraglomerular cells including podocytes, glomerular endothelial cells (GECs) and mesangial cells (MCs), the alterations in one cell type can produce changes in the others. The cell-to-cell crosstalk plays a crucial role in maintaining the glomerular filtration barrier (GFB) and homeostasis. In this review, we summarized the recent advances in understanding the pathological changes and interactions of these three types of cells in DKD and then focused on the signaling pathways and factors that mediate the crosstalk, such as angiopoietins, vascular endothelial growth factors, transforming growth factor-β, Krüppel-like factors, retinoic acid receptor response protein 1 and exosomes, etc. Furthermore, we also simply introduce the application of the latest technologies in studying cell interactions within glomerular cells and new promising mediators for cell crosstalk in DKD. In conclusion, this review provides a comprehensive and updated overview of the glomerular crosstalk in DKD and highlights its importance for the development of novel intervention approaches.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38374141 · DOI · PMC10875896
Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The glomerular filtration barrier, comprising the inner layer of capillary fenestrated endothelial cells, outermost podocytes, and the glomerular basement membrane between them, plays a pivotal role in kidney function.
- Closing excerpt
- It offers valuable insights for a deeper understanding of the role of podocytes in proteinuric glomerular diseases, and the identification of new therapeutic targets, and has significant implications for the future clinical diagnosis and treatment of podocyte-related disorders.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (223 words)
The glomerular filtration barrier, comprising the inner layer of capillary fenestrated endothelial cells, outermost podocytes, and the glomerular basement membrane between them, plays a pivotal role in kidney function. Podocytes, terminally differentiated epithelial cells, are challenging to regenerate once injured. They are essential for maintaining the integrity of the glomerular filtration barrier. Damage to podocytes, resulting from intrinsic or extrinsic factors, leads to proteinuria in the early stages and eventually progresses to chronic kidney disease (CKD). Immune-mediated podocyte injury is a primary pathogenic mechanism in proteinuric glomerular diseases, including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, and lupus nephritis with podocyte involvement. An extensive body of evidence indicates that podocytes not only contribute significantly to the maintenance of the glomerular filtration barrier and serve as targets of immune responses but also exhibit immune cell-like characteristics, participating in both innate and adaptive immunity. They play a pivotal role in mediating glomerular injury and represent potential therapeutic targets for CKD. This review aims to systematically elucidate the mechanisms of podocyte immune injury in various podocyte lesions and provide an overview of recent advances in podocyte immunotherapy. It offers valuable insights for a deeper understanding of the role of podocytes in proteinuric glomerular diseases, and the identification of new therapeutic targets, and has significant implications for the future clinical diagnosis and treatment of podocyte-related disorders.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38288116 · DOI · PMC10822972
Renal Angptl4 is a key fibrogenic molecule in progressive diabetic kidney disease [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Angiopoietin-like 4 (ANGPTL4), a key protein involved in lipoprotein metabolism, has diverse effects.
- Closing excerpt
- Together, these data demonstrate that podocyte- and tubule-derived Angptl4 is fibrogenic in diabetic kidneys.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (158 words)
Angiopoietin-like 4 (ANGPTL4), a key protein involved in lipoprotein metabolism, has diverse effects. There is an association between Angptl4 and diabetic kidney disease; however, this association has not been well investigated. We show that both podocyte- and tubule-specific ANGPTL4 are crucial fibrogenic molecules in diabetes. Diabetes accelerates the fibrogenic phenotype in control mice but not in ANGPTL4 mutant mice. The protective effect observed in ANGPTL4 mutant mice is correlated with a reduction in stimulator of interferon genes pathway activation, expression of pro-inflammatory cytokines, reduced epithelial-to-mesenchymal transition and endothelial-to-mesenchymal transition, lessened mitochondrial damage, and increased fatty acid oxidation. Mechanistically, we demonstrate that podocyte- or tubule-secreted Angptl4 interacts with Integrin β1 and influences the association between dipeptidyl-4 with Integrin β1. We demonstrate the utility of a targeted pharmacologic therapy that specifically inhibits Angptl4 gene expression in the kidneys and protects diabetic kidneys from proteinuria and fibrosis. Together, these data demonstrate that podocyte- and tubule-derived Angptl4 is fibrogenic in diabetic kidneys.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39630889 · DOI · PMC11616692
SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3 [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Podocyte dysfunction represents both an early pathological hallmark and a key driver of proteinuria in diabetic kidney disease (DKD); nevertheless, the potential epigenetic regulatory mechanisms remain poorly defined.
- Closing excerpt
- Collectively, these findings establish SETDB2 as a critical regulator of podocyte integrity and a promising therapeutic target for DKD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
Podocyte dysfunction represents both an early pathological hallmark and a key driver of proteinuria in diabetic kidney disease (DKD); nevertheless, the potential epigenetic regulatory mechanisms remain poorly defined. Here, the histone methyltransferase SETDB2 is identified as a pivotal epigenetic suppressor of podocyte dysfunction and DKD progression. Glomerular SETDB2 expression exhibits a significant reduce in both DKD patients and mouse models, showing an inverse correlation with disease severity. Podocyte-specific SETDB2 deficiency exacerbates podocytes dysfunction and accelerates DKD progression, whereas its overexpression exerts renal protective effects. Mechanistically, SETDB2 directly enhances H3K9 trimethylation at the Smad3 promoter, thereby repressing SMAD3 expression and activation, ultimately preserving podocyte function. Notably, it identifies TCF21, a transcription factor downregulated in DKD, as a direct upstream regulator of Setdb2 expression via binding to promoter and activating its transcription. Collectively, these findings establish SETDB2 as a critical regulator of podocyte integrity and a promising therapeutic target for DKD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41316884 · DOI · PMC12904062
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Podocytopathies [5]
- Research article Podocyte injury and its consequences [6]
- Research article Actin up: regulation of podocyte structure and function by components of the actin cytoskeleton [7]
- Research article Molecular pathways that drive diabetic kidney disease [8]
- Research article Differentiating Primary, Genetic, and Secondary FSGS in Adults: A Clinicopathologic Approach [9]
- Research article The podocyte slit diaphragm--from a thin grey line to a complex signalling hub [10]
References
- Hu S, Hang X, Wei Y, Wang H, Zhang L, Zhao L. Crosstalk among podocytes, glomerular endothelial cells and mesangial cells in diabetic kidney disease: an updated review. . 2024. PMID 38374141 · DOI · PMC10875896
- Jiang H, Shen Z, Zhuang J, Lu C, Qu Y, Xu C, et al.. Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy. . 2023. PMID 38288116 · DOI · PMC10822972
- Srivastava SP, Zhou H, Shenoi R, Morris M, Lainez-Mas B, Goedeke L, et al.. Renal Angptl4 is a key fibrogenic molecule in progressive diabetic kidney disease. . 2024. PMID 39630889 · DOI · PMC11616692
- Li L, Jiang S, Jin Q, Qu P, Guo Y, Lan X, et al.. SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3. . 2026. PMID 41316884 · DOI · PMC12904062
- Kopp JB, Anders HJ, Susztak K, Podestà MA, Remuzzi G, Hildebrandt F, et al.. Podocytopathies. Nat Rev Dis Primers. 2020. PMID 32792490 · DOI · PMC8162925
- Nagata M. Podocyte injury and its consequences. Kidney Int. 2016. PMID 27165817 · DOI
- Faul C, Asanuma K, Yanagida-Asanuma E, Kim K, Mundel P. Actin up: regulation of podocyte structure and function by components of the actin cytoskeleton. Trends Cell Biol. 2007. PMID 17804239 · DOI
- Mohandes S, Doke T, Hu H, Mukhi D, Dhillon P, Susztak K. Molecular pathways that drive diabetic kidney disease. J Clin Invest. 2023. PMID 36787250 · DOI · PMC9927939
- De Vriese AS, Sethi S, Nath KA, Glassock RJ, Fervenza FC. Differentiating Primary, Genetic, and Secondary FSGS in Adults: A Clinicopathologic Approach. J Am Soc Nephrol. 2018. PMID 29321142 · DOI · PMC5827609
- Grahammer F, Schell C, Huber TB. The podocyte slit diaphragm--from a thin grey line to a complex signalling hub. Nat Rev Nephrol. 2013. PMID 23999399 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.