ArticleJCI insight2019
mTOR-mediated podocyte hypertrophy regulates glomerular integrity in mice and humans.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 100 citations in OpenAlex.
- Metabolic surgery mitigates early kidney injury in obese youth with diabetes by suppressing mTORC1/JAK/STAT signaling.The Journal of clinical investigation · 2026Trial
- Review
- Mechanisms of Podocyte Injury in Kidney Allografts.Kidney360 · 2026Review
- AMPK is dispensable for physiological podocyte and glomerular functions but prevents glomerular fibrosis in experimental diabetes.Cell death discovery · 2026Article
- Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026Review
- Innovative Technologies for Kidney Research: Three-Dimensional Imaging and Quantification.Seminars in nephrology · 2026Review
- Sexual Dimorphism in Renal Progenitors: Do Immunosuppressants Erase the Female Advantage?Transplant international : official journal of the European Society for Organ Transplantation · 2026Article
- Podocytes in health and disease: from development to regeneration.Human cell · 2025Review
- The intelligent podocyte: sensing and responding to a complex microenvironment.Nature reviews. Nephrology · 2025Review
- Loss of genome maintenance is linked to mTOR complex 1 signaling and accelerates podocyte damage.JCI insight · 2025Article
- The growth hormone/IGF-1 axis is a risk factor for long-term kidney allograft failure.JCI insight · 2025Article
- Preterm birth increases susceptibility to hyperglycemia induced glomerular alterations in male mice.Scientific reports · 2025Article
- Transcriptional Regulators YAP and TAZ Have Distinct Abilities to Compensate for One Another in Podocytes.Journal of the American Society of Nephrology : JASN · 2025Article
- mTOR pathway: A key player in diabetic nephropathy progression and therapeutic targets.Genes & diseases · 2025Review
- Targeting lipid metabolic reprogramming to alleviate diabetic kidney disease: molecular insights and therapeutic strategies.Frontiers in immunology · 2025Review
- mTORC1 signaling and diabetic kidney disease.Diabetology international · 2024Review
- Sex-specific molecular signature of mouse podocytes in homeostasis and in response to pharmacological challenge with rapamycin.Biology of sex differences · 2024Article
- Review
- PIK3CA inhibition in models of proliferative glomerulonephritis and lupus nephritis.The Journal of clinical investigation · 2024Article
- Role of biophysics and mechanobiology in podocyte physiology.Nature reviews. Nephrology · 2024Review
Corrections and comments
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Authors and funding
33 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cellular origins of glomerulosclerosis involve activation of parietal epithelial cells (PECs) and progressive podocyte depletion. While mammalian target of rapamycin-mediated (mTOR-mediated) podocyte hypertrophy is recognized as an important signaling pathway in the context of glomerular disease, the role of podocyte hypertrophy as a compensatory mechanism preventing PEC activation and glomerulosclerosis remains poorly understood. In this study, we show that glomerular mTOR and PEC activation-related genes were both upregulated and intercorrelated in biopsies from patients with focal segmental glomerulosclerosis (FSGS) and diabetic nephropathy, suggesting both compensatory and pathological roles. Advanced morphometric analyses in murine and human tissues identified podocyte hypertrophy as a compensatory mechanism aiming to regulate glomerular functional integrity in response to somatic growth, podocyte depletion, and even glomerulosclerosis - all of this in the absence of detectable podocyte regeneration. In mice, pharmacological inhibition of mTOR signaling during acute podocyte loss impaired hypertrophy of remaining podocytes, resulting in unexpected albuminuria, PEC activation, and glomerulosclerosis. Exacerbated and persistent podocyte hypertrophy enabled a vicious cycle of podocyte loss and PEC activation, suggesting a limit to its beneficial effects. In summary, our data highlight a critical protective role of mTOR-mediated podocyte hypertrophy following podocyte loss in order to preserve glomerular integrity, preventing PEC activation and 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.