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 (660 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
Smooth muscle-like cells adhering to the wall of the small blood vessels of the kidney at the glomerulus and along the vascular pole of the glomerulus in the juxtaglomerular apparatus. They are myofibroblasts with contractile and phagocytic properties. These cells and their mesangial extracellular matrix constitute the glomerular mesangium.
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: Cell, Mesangial; Cells, Mesangial; Mesangial Cell; Mesangial Cells, Kidney; Cell, Kidney Mesangial; Cells, Kidney Mesangial; Kidney Mesangial Cell; Kidney Mesangial Cells.
Where it fits in the MeSH classification
- Broader topics
- Kidney Glomerulus; Fibroblasts
- Narrower topics
- Glomerular Mesangium
Related concepts
- Kidney
- Juxtaglomerular Apparatus
- Mesangial Extracellular Matrix
- Glomerular Mesangium
Research landscape
PubMed indexes 7,893 records tagged with the MeSH heading “Mesangial Cells” (counts retrieved 2026-10-31). 565 of them (7.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 3,324 records.
Reviews account for 633 records (8.0%) and meta-analyses for 2. Randomized controlled trials number 14 (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 | 3,324 |
| 2000-2009 | 2,313 |
| 2010-2019 | 1,691 |
| 2020 onward | 565 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 633 | 8.0% |
| Meta-analyses | 2 | 0.0% |
| Randomized controlled trials | 14 | 0.2% |
Method: PubMed query "Mesangial Cells"[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 |
|---|---|---|---|---|
| Targeted delivery of celastrol to mesangial cells is effective against mesangioproliferative glomerulonephritis | 2017 | Research article Design not recorded in structured metadata | 175 | cc by PMID 29026082 · DOI · PMC5638829 |
| HMGB1 regulates ferroptosis through Nrf2 pathway in mesangial cells in response to high glucose | 2021 | Research article Design not recorded in structured metadata | 160 | cc by PMID 33565572 · DOI · PMC7897919 |
| High Glucose and Lipopolysaccharide Prime NLRP3 Inflammasome via ROS/TXNIP Pathway in Mesangial Cells | 2016 | Research article Design not recorded in structured metadata | 104 | cc by PMID 26881256 · DOI · PMC4736396 |
| Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications | 2025 | Review article Design not recorded in structured metadata | 26 | cc by PMID 40860185 · DOI · PMC12374811 |
Targeted delivery of celastrol to mesangial cells is effective against mesangioproliferative glomerulonephritis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Mesangial cells-mediated glomerulonephritis is a frequent cause of end-stage renal disease.
- Closing excerpt
- Here the authors show that celastrol loaded in albumin nanoparticles efficiently targets mesangial cells, and is effective in rat models.
- 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 (137 words)
Mesangial cells-mediated glomerulonephritis is a frequent cause of end-stage renal disease. Here, we show that celastrol is effective in treating both reversible and irreversible mesangioproliferative glomerulonephritis in rat models, but find that its off-target distributions cause severe systemic toxicity. We thus target celastrol to mesangial cells using albumin nanoparticles. Celastrol-albumin nanoparticles crosses fenestrated endothelium and accumulates in mesangial cells, alleviating proteinuria, inflammation, glomerular hypercellularity, and excessive extracellular matrix deposition in rat anti-Thy1.1 nephritis models. Celastrol-albumin nanoparticles presents lower drug accumulation than free celastrol in off-target organs and tissues, thereby minimizing celastrol-related systemic toxicity. Celastrol-albumin nanoparticles thus represents a promising treatment option for mesangioproliferative glomerulonephritis and similar glomerular diseases.Mesangial cell-mediated glomerulonephritis is a frequent cause of kidney disease. Here the authors show that celastrol loaded in albumin nanoparticles efficiently targets mesangial cells, and is effective in rat models.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29026082 · DOI · PMC5638829
HMGB1 regulates ferroptosis through Nrf2 pathway in mesangial cells in response to high glucose [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Ferroptosis, a novel type of programmed cell death, is involved in inflammation and oxidation of various human diseases, including diabetic kidney disease.
- Closing excerpt
- Collectively, these findings suggest that HMGB1 regulates glucose-induced ferroptosis via Nrf2 pathway in mesangial cells.
- 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 (197 words)
Ferroptosis, a novel type of programmed cell death, is involved in inflammation and oxidation of various human diseases, including diabetic kidney disease. The present study explored the role of high-mobility group box-1 (HMGB1) on the regulation of ferroptosis in mesangial cells in response to high glucose. Compared with healthy control, levels of serum ferritin, lactate dehydrogenase (LDH), reactive oxygen species (ROS), malonaldehyde (MDA), and HMGB1 were significantly elevated in diabetic nephropathy (DN) patients, accompanied with deregulated ferroptosis-related molecules, including long-chain acyl-CoA synthetase 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (PTGS2), NADPH oxidase 1 (NOX1), and glutathione peroxidase 4 (GPX4). In vitro assay revealed that erastin and high glucose both induced ferroptosis in mesangial cells. Suppression of HMGB1 restored cellular proliferation, prevented ROS and LDH generation, decreased ACSL4, PTGS2, and NOX1, and increased GPX4 levels in mesangial cells. Furthermore, nuclear factor E2-related factor 2 (Nrf2) was decreased in DN patients and high glucose-mediated translocation of HMGB1 in mesangial cells. Knockdown of HMGB1 suppressed high glucose-induced activation of TLR4/NF-κB axis and promoted Nrf2 expression as well as its downstream targets including HO-1, NQO-1, GCLC, and GCLM. Collectively, these findings suggest that HMGB1 regulates glucose-induced ferroptosis via Nrf2 pathway in mesangial cells.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33565572 · DOI · PMC7897919
High Glucose and Lipopolysaccharide Prime NLRP3 Inflammasome via ROS/TXNIP Pathway in Mesangial Cells [3]
Abstract reading summary — source excerpts
- Opening excerpt
- While inflammation is considered a central component in the development in diabetic nephropathy, the mechanism remains unclear.
- Closing excerpt
- Our results firstly reveal that high glucose and lipopolysaccharide activate ROS/TXNIP/ NLRP3/IL-1β inflammasome signaling in glomerular mesangial cells, suggesting a mechanism by which inflammation may contribute to the development of diabetic nephropathy.
- 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 (195 words)
While inflammation is considered a central component in the development in diabetic nephropathy, the mechanism remains unclear. The NLRP3 inflammasome acts as both a sensor and a regulator of the inflammatory response. The NLRP3 inflammasome responds to exogenous and endogenous danger signals, resulting in cleavage of procaspase-1 and activation of cytokines IL-1β, IL-18, and IL-33, ultimately triggering an inflammatory cascade reaction. This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy. We found that the expression of thioredoxin-interacting protein (TXNIP), NLRP3, and IL-1β was observed by immunohistochemistry in vivo. Simultaneously, the mRNA and protein levels of TXNIP, NLRP3, procaspase-1, and IL-1β were significantly induced by high glucose concentration and lipopolysaccharide in a dose-dependent and time-dependent manner in vitro. This induction by both high glucose and lipopolysaccharide was significantly inhibited by N-acetyl-L-cysteine. Our results firstly reveal that high glucose and lipopolysaccharide activate ROS/TXNIP/ NLRP3/IL-1β inflammasome signaling in glomerular mesangial cells, suggesting a mechanism by which inflammation may contribute to the development of diabetic nephropathy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26881256 · DOI · PMC4736396
Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Diabetic kidney disease (DKD) is a serious diabetic complication, the morbidity and mortality of which has rapidly increased worldwide.
- Closing excerpt
- In this review, we summarize and outline the mechanisms of MC injury and the interactions of MCs with other cells and discuss the progress of MC-targeted therapeutics to provide a comprehensive perspective on the prevention and treatment of 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 (131 words)
Diabetic kidney disease (DKD) is a serious diabetic complication, the morbidity and mortality of which has rapidly increased worldwide. As known, the pathogenesis of DKD is complex and includes mesangial cell (MC) proliferation and hypertrophy, mesangial expansion, glomerular basement membrane thickening, podocyte detachment, and tubulointerstitial damage. Thus, the role of MCs cannot be underestimated, as their exclusive positioning and diverse physiological functions are crucial for preserving the glomerular filtration membrane's composition and functionality. Considerable animal studies and clinical trials have elaborated that MCs are pivotal to the occurrence and progression of DKD. In this review, we summarize and outline the mechanisms of MC injury and the interactions of MCs with other cells and discuss the progress of MC-targeted therapeutics to provide a comprehensive perspective on the prevention and treatment of DKD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40860185 · DOI · PMC12374811
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 Extracellular matrix metabolism in diabetic nephropathy [5]
- Research article From the periphery of the glomerular capillary wall toward the center of disease: podocyte injury comes of age in diabetic nephropathy [6]
- Research article The mesangial cell revisited: no cell is an island [7]
- Research article Physiology of the mesangial cell [8]
- Research article The glomerular mesangial cell: an expanding role for a specialized pericyte [9]
- Research article Transforming growth factor-beta regulates production of proteoglycans by mesangial cells [10]
References
- Guo L, Luo S, Du Z, Zhou M, Li P, Fu Y, et al.. Targeted delivery of celastrol to mesangial cells is effective against mesangioproliferative glomerulonephritis. . 2017. PMID 29026082 · DOI · PMC5638829
- Wu Y, Zhao Y, Yang HZ, Wang YJ, Chen Y. HMGB1 regulates ferroptosis through Nrf2 pathway in mesangial cells in response to high glucose. . 2021. PMID 33565572 · DOI · PMC7897919
- Feng H, Gu J, Gou F, Huang W, Gao C, Chen G, et al.. High Glucose and Lipopolysaccharide Prime NLRP3 Inflammasome via ROS/TXNIP Pathway in Mesangial Cells. . 2016. PMID 26881256 · DOI · PMC4736396
- Feng L, Feng YY, Ren Q, Fu P, Ma L. Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications. . 2025. PMID 40860185 · DOI · PMC12374811
- Mason RM, Wahab NA. Extracellular matrix metabolism in diabetic nephropathy. J Am Soc Nephrol. 2003. PMID 12707406 · DOI
- Wolf G, Chen S, Ziyadeh FN. From the periphery of the glomerular capillary wall toward the center of disease: podocyte injury comes of age in diabetic nephropathy. Diabetes. 2005. PMID 15919782 · DOI
- Schlöndorff D, Banas B. The mesangial cell revisited: no cell is an island. J Am Soc Nephrol. 2009. PMID 19470685 · DOI
- Mené P, Simonson MS, Dunn MJ. Physiology of the mesangial cell. Physiol Rev. 1989. PMID 2678170 · DOI
- Schlondorff D. The glomerular mesangial cell: an expanding role for a specialized pericyte. FASEB J. 1987. PMID 3308611 · DOI
- Border WA, Okuda S, Languino LR, Ruoslahti E. Transforming growth factor-beta regulates production of proteoglycans by mesangial cells. Kidney Int. 1990. PMID 2407884 · 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.