ArticleJournal of hypertension2019
Coexisting renal artery stenosis and metabolic syndrome magnifies mitochondrial damage, aggravating poststenotic kidney injury in pigs.
Article in Journal of hypertension, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 20 citations in OpenAlex.
- Renovascular Disease and Its Impact on Endogenous Kidney Repair: Stem/Progenitor Cells.Stem cells international · 2026Review
- Article
- Contemporary Perspectives on Chronic Renal Disorders.Chronic diseases and translational medicine · 2025Review
- Role of mitochondria in endogenous renal repair.Clinical science (London, England : 1979) · 2024Review
- Article
- Metabolic phenotypes and risk of end-stage kidney disease in patients with type 2 diabetes.Frontiers in endocrinology · 2023Article
- Article
- Prognostic value of metabolic syndrome in renal structural changes in type 2 diabetes.International urology and nephrology · 2022Article
- Article
- Renal mitochondrial injury in the pathogenesis of CKD: mtDNA and mitomiRs.Clinical science (London, England : 1979) · 2022Review
- Renal Revascularization Attenuates Myocardial Mitochondrial Damage and Improves Diastolic Function in Pigs with Metabolic Syndrome and Renovascular Hypertension.Journal of cardiovascular translational research · 2022Article
- Percutaneous transluminal renal angioplasty attenuates poststenotic kidney mitochondrial damage in pigs with renal artery stenosis and metabolic syndrome.Journal of cellular physiology · 2021Article
- Renovascular Hypertension Induces Myocardial Mitochondrial Damage, Contributing to Cardiac Injury and Dysfunction in Pigs With Metabolic Syndrome.American journal of hypertension · 2021Article
- Metabolic Syndrome Impairs 3D Mitochondrial Structure, Dynamics, and Function in Swine Mesenchymal Stem Cells.Stem cell reviews and reports · 2020Article
- Experimental Renovascular Disease Induces Endothelial Cell Mitochondrial Damage and Impairs Endothelium-Dependent Relaxation of Renal Artery Segments.American journal of hypertension · 2020Article
- Renal ischemia alters expression of mitochondria-related genes and impairs mitochondrial structure and function in swine scattered tubular-like cells.American journal of physiology. Renal physiology · 2020Article
- Metabolic Syndrome Alters the Cargo of Mitochondria-Related microRNAs in Swine Mesenchymal Stem Cell-Derived Extracellular Vesicles, Impairing Their Capacity to Repair the Stenotic Kidney.Stem cells international · 2020Article
- Renovascular disease induces mitochondrial damage in swine scattered tubular cells.American journal of physiology. Renal physiology · 2019Article
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
objectiveRenovascular disease (RVD) produces chronic underperfusion of the renal parenchyma and progressive ischemic injury. Metabolic abnormalities often accompany renal ischemia, and are linked to poorer renal outcomes. However, the mechanisms of injury in kidneys exposed to the ischemic and metabolic components of RVD are incompletely understood. We hypothesized that coexisting renal artery stenosis (RAS) and metabolic syndrome (MetS) would exacerbate mitochondrial damage, aggravating poststenotic kidney injury in swine.
methodsDomestic pigs were studied after 16 weeks of either standard diet (Lean) or high-fat/high-fructose (MetS) with or without superimposed RAS (n = 6 each). Single-kidney renal blood flow (RBF) and glomerular filtration rate (GFR) were assessed in vivo with multidetector-CT, and renal tubular mitochondrial structure, homeostasis and function and renal injury ex vivo.
resultsBoth RAS groups achieved significant stenosis. Single-kidney RBF and GFR were higher in MetS compared with Lean, but decreased in Lean+RAS and MetS+RAS vs. their respective controls. MetS and RAS further induced changes in mitochondrial structure, dynamics, and function, and their interaction (diet × ischemia) decreased matrix density, mitophagy, and ATP production, and lead to greater renal fibrosis.
conclusionCoexisting RAS and MetS synergistically aggravate mitochondrial structural damage and dysfunction, which may contribute to structural injury and dysfunction in the poststenotic kidney. These observations suggest that mitochondrial damage precedes loss of renal function in experimental RVD, and position mitochondria as novel therapeutic targets in these patients.
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