ArticleAmerican journal of physiology. Renal physiology2014
Mpv17 in mitochondria protects podocytes against mitochondrial dysfunction and apoptosis in vivo and in vitro.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 53 citations in OpenAlex.
- Podocyte-derived endothelin-1 and endothelial cell endothelin A receptors are essential for glomerular injury in mouse models of focal segmental glomerulosclerosis.Kidney international · 2026Article
- Mitochondrial Homeostasis in Pancreatic β Cell Function: Mechanisms and Therapeutic Targets for Diabetes.Journal of diabetes · 2026Review
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- Metabolic syndrome and kidney dysfunction: emerging molecular and cellular mechanisms at the metabolic-renal interface.Frontiers in endocrinology · 2026Review
- Oxidative Stress and Nutritional Antioxidants in Renal Diseases: A Narrative Review.Antioxidants (Basel, Switzerland) · 2025Review
- Precision Prediction of Alzheimer's Disease: Integrating Mitochondrial Energy Metabolism and Immunological Insights.Journal of molecular neuroscience : MN · 2025Article
- Icariin ameliorates minimal change disease by regulating the mitochondrial dysfunction pathway: an integrated strategy of network pharmacology, bioinformatics, and experimental validation.Frontiers in pharmacology · 2025Article
- Mitochondrial protein MPV17 promotes β-cell apoptosis in diabetogenesis.Clinical science (London, England : 1979) · 2023Article
- Identification and validation of potential biomarkers for atrial fibrillation based on integrated bioinformatics analysis.Frontiers in cell and developmental biology · 2023Article
- Overexpression mutants reveal a role for a chloroplast MPD protein in regulation of reactive oxygen species during chilling in Arabidopsis.Journal of experimental botany · 2022Article
- Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022Article
- A Deep Insight Into Regulatory T Cell Metabolism in Renal Disease: Facts and Perspectives.Frontiers in immunology · 2022Review
- The IRE1α pathway in glomerular diseases: The unfolded protein response and beyond.Frontiers in molecular medicine · 2022Review
- The glomerular filtration barrier: a structural target for novel kidney therapies.Nature reviews. Drug discovery · 2021Review
- Jianpi Qushi Heluo Formula alleviates renal damages in Passive Hemann nephritis in rats by upregulating Parkin-mediated mitochondrial autophagy.Scientific reports · 2021Article
- MPV17 Mutations Are Associated With a Quiescent Energetic Metabolic Profile.Frontiers in cellular neuroscience · 2021Article
- Role of IRE1α in podocyte proteostasis and mitochondrial health.Cell death discovery · 2020Article
- New In Vitro Model of Oxidative Stress: Human Prostate Cells Injured with 2,2-diphenyl-1-picrylhydrazyl (DPPH) for the Screening of Antioxidants.International journal of molecular sciences · 2020Article
- Mitochondria Matter: A Critical Role ofJournal of the American Society of Nephrology : JASN · 2020Article
- A mitochondrial-targeted peptide ameliorated podocyte apoptosis through a HOCl-alb-enhanced and mitochondria-dependent signalling pathway in diabetic rats and in vitro.Journal of enzyme inhibition and medicinal chemistry · 2019Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Mitochondrial dysfunction is increasingly recognized as contributing to glomerular diseases, including those secondary to mitochondrial DNA (mtDNA) mutations and deletions. Mitochondria maintain cellular redox and energy homeostasis and are a major source of intracellular reactive oxygen species (ROS) production. Mitochondrial ROS accumulation may contribute to stress-induced mitochondrial dysfunction and apoptosis and thereby to glomerulosclerosis. In mice, deletion of the gene encoding Mpv17 is associated with glomerulosclerosis, but the underlying mechanism remains poorly defined. Here we report that Mpv17 localizes to mitochondria of podocytes and its expression is reduced in several glomerular injury models and in human focal segmental glomerulosclerosis (FSGS) but not in minimal change disease. Using models of mild or severe nephrotoxic serum nephritis (NTSN) in Mpv17(+/+) wild-type (WT) and Mpv17(-/-) knockout mice, we found that Mpv17 deficiency resulted in increased proteinuria (mild NTSN) and renal insufficiency (severe NTSN) compared with WT. These lesions were associated with increased mitochondrial ROS generation and mitochondrial injury such as oxidative DNA damage. In vitro, podocytes with loss of Mpv17 function were characterized by increased susceptibility to apoptosis and ROS injury including decreased mitochondrial function, loss of mtDNA content, and change in mitochondrial configuration. In summary, the inner mitochondrial membrane protein Mpv17 in podocytes is essential for the maintenance of mitochondrial homeostasis and protects podocytes against oxidative stress-induced injury both in vitro and in vivo.
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