ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS2015
ACE-inhibition increases podocyte number in experimental glomerular disease independent of proliferation.
Article in Journal of the renin-angiotensin-aldosterone system : JRAAS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Clinical spectrum, genetics and management insights of PAX2-related disorder in nine children.European journal of medical research · 2025Article
- Blood Pressure Management Strategies and Podocyte Health.American journal of hypertension · 2025Review
- Podocyte-Related Mechanisms Underlying Survival Benefit of Long-Term Angiotensin Receptor Blocker.International journal of molecular sciences · 2022Article
- The Pathology Lesion Patterns of Podocytopathies: How and why?Frontiers in cell and developmental biology · 2022Review
- Drug Testing for Residual Progression of Diabetic Kidney Disease in Mice Beyond Therapy with Metformin, Ramipril, and Empagliflozin.Journal of the American Society of Nephrology : JASN · 2020Article
- Glucocorticoids in the treatment of patients with primary focal segmental glomerulosclerosis and moderate proteinuria.Clinical and experimental nephrology · 2018Article
- Cells of NG2 lineage increase in glomeruli of mice following podocyte depletion.American journal of physiology. Renal physiology · 2018Article
- Proteinuric Kidney Diseases: A Podocyte's Slit Diaphragm and Cytoskeleton Approach.Frontiers in medicine · 2018Review
- Lysophosphatidic Acid Receptor Antagonism Protects against Diabetic Nephropathy in a Type 2 Diabetic Model.Journal of the American Society of Nephrology : JASN · 2017Article
- WT1 Is Necessary for the Proliferation and Migration of Cells of Renin Lineage Following Kidney Podocyte Depletion.Stem cell reports · 2017Article
- Can podocytes be regenerated in adults?Current opinion in nephrology and hypertension · 2017Review
- Activated ERK1/2 increases CD44 in glomerular parietal epithelial cells leading to matrix expansion.Kidney international · 2017Article
- Tracking the stochastic fate of cells of the renin lineage after podocyte depletion using multicolor reporters and intravital imaging.PloS one · 2017Article
- Renin-Angiotensin-Aldosterone System Inhibition Increases Podocyte Derivation from Cells of Renin Lineage.Journal of the American Society of Nephrology : JASN · 2016Article
- Reducing mTOR augments parietal epithelial cell density in a model of acute podocyte depletion and in aged kidneys.American journal of physiology. Renal physiology · 2016Article
- Partial podocyte replenishment in experimental FSGS derives from nonpodocyte sources.American journal of physiology. Renal physiology · 2016Article
- G Protein-Coupled Bile Acid Receptor TGR5 Activation Inhibits Kidney Disease in Obesity and Diabetes.Journal of the American Society of Nephrology : JASN · 2016Article
- Cells of renin lineage express hypoxia inducible factor 2α following experimental ureteral obstruction.BMC nephrology · 2016Article
- Glomerular parietal epithelial cells contribute to adult podocyte regeneration in experimental focal segmental glomerulosclerosis.Kidney international · 2015Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveThe objective of this article is to test the effects of angiotensin-converting enzyme (ACE)-inhibition on glomerular epithelial cell number in an inducible experimental model of focal segmental glomerulosclerosis (FSGS).
backgroundAlthough ACE-inhibition has been shown to limit podocyte loss by enhancing survival, little is known about its effect on podocyte number following an abrupt decline in disease.
methodsExperimental FSGS was induced with cytotoxic antipodocyte antibody. Following induction, groups were randomized to receive the ACE-inhibitor enalapril, the smooth muscle relaxant hydralazine (blood pressure control) or drinking water. Blood pressure, kidney function and histology were measured seven and 14 days following disease induction.
resultsBoth glomerulosclerosis and urinary albumin-to-creatinine ratio were less in the ACE-inhibition arm at day 14. At day 7 of disease, mean podocyte numbers were 26% and 29% lower in the enalapril and hydralazine arms, respectively, compared to normal mice in which no antibody was injected. At day 14, the mean podocyte number was only 18% lower in the enalapril arm, but was 39% lower in the hydralazine arm compared to normal mice. Podocyte proliferation did not occur at any time in any group. Compared to water- or hydralazine-treated mice with FSGS, the enalapril arm had a higher mean number of glomerular parietal epithelial cells that co-expressed the podocyte proteins WT-1 and synaptopodin, as well as phospho-ERK.
conclusionThe results show following an abrupt decline in podocyte number, the initiation of ACE-inhibition but not hydralazine, was accompanied by higher podocyte number in the absence of proliferation. This was accompanied by a higher number of parietal epithelial cells that co-express podocyte proteins. Increasing podocyte number appears to be accompanied by reduced glomerulosclerosis.
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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 OpenQuestion graph.