ArticleTranslational research : the journal of laboratory and clinical medicine2017
The metabolic syndrome induces early changes in the swine renal medullary mitochondria.
Article in Translational research : the journal of laboratory and clinical medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 32 citations in OpenAlex.
- The effect of weight-loss surgery in patients with obesity on adipose tissue mesenchymal stem cells versus circulating endothelial progenitor cells.International journal of obesity (2005) · 2026Article
- Nanomedicines Against Mitochondrial Dysfunction-Induced Metabolic Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Renal Ischemia Induces Endoplasmic Reticulum Stress and Impairs the Reparative Potency of Scattered Tubular-Like Cells.American journal of nephrology · 2025Article
- Metabolic phenotypes and risk of end-stage kidney disease in patients with type 2 diabetes.Frontiers in endocrinology · 2023Article
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- Cardiac micro-RNA and transcriptomic profile of a novel swine model of chronic kidney disease and left ventricular diastolic dysfunction.American journal of physiology. Heart and circulatory physiology · 2022Article
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- Article
- Renal mitochondrial injury in the pathogenesis of CKD: mtDNA and mitomiRs.Clinical science (London, England : 1979) · 2022Review
- SS-31, a Mitochondria-Targeting Peptide, Ameliorates Kidney Disease.Oxidative medicine and cellular longevity · 2022Review
- Percutaneous transluminal renal angioplasty attenuates poststenotic kidney mitochondrial damage in pigs with renal artery stenosis and metabolic syndrome.Journal of cellular physiology · 2021Article
- 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
- Renal Adiposity Does not Preclude Quantitative Assessment of Renal Function Using Dual-Energy Multidetector CT in Mildly Obese Human Subjects.Academic radiology · 2019Article
- Renovascular disease induces mitochondrial damage in swine scattered tubular cells.American journal of physiology. Renal physiology · 2019Article
- Coexisting renal artery stenosis and metabolic syndrome magnifies mitochondrial damage, aggravating poststenotic kidney injury in pigs.Journal of hypertension · 2019Article
- Early podocyte injury and elevated levels of urinary podocyte-derived extracellular vesicles in swine with metabolic syndrome: role of podocyte mitochondria.American journal of physiology. Renal physiology · 2019Article
- Urinary mitochondrial DNA copy number identifies renal mitochondrial injury in renovascular hypertensive patients undergoing renal revascularization: A Pilot Study.Acta physiologica (Oxford, England) · 2019Article
- Mitochondrial Protection Partly Mitigates Kidney Cellular Senescence in Swine Atherosclerotic Renal Artery Stenosis.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The metabolic syndrome (MetS) is associated with nutrient surplus and kidney hyperfiltration, accelerating chronic renal failure. Mitochondria can be overwhelmed by substrate excess, leading to inefficient energy production and thereby tissue hypoxia. Mitochondrial dysfunction is emerging as an important determinant of renal damage, but whether it contributes to MetS-induced renal injury remains unknown. We hypothesized that early MetS induces kidney mitochondrial abnormalities and dysfunction, which would be notable in the vulnerable renal medulla. Pigs were studied after 16 weeks of diet-induced MetS, MetS treated for the last 4 weeks with the mitochondria-targeted peptide elamipretide (0.1 mg/kg SC q.d), and Lean controls (n = 7 each). Single-kidney renal blood flow, glomerular filtration rate, and oxygenation were measured in-vivo, whereas cortical and medullary mitochondrial structure and function and renal injurious pathways were studied ex-vivo. Blood pressure was slightly elevated in MetS pigs, and their renal blood flow and glomerular filtration rate were elevated. Blood oxygen level-dependent magnetic resonance imaging demonstrated that this was associated with medullary hypoxia, whereas cortical oxygenation remained intact. MetS decreased renal content of the inner mitochondrial membrane cardiolipin, particularly the tetra-linoleoyl (C18:2) cardiolipin species, and altered mitochondrial morphology and function, particularly in the medullary thick ascending limb. MetS also increased renal cytochrome-c-induced apoptosis, oxidative stress, and tubular injury. Chronic mitoprotection restored mitochondrial structure, ATP synthesis, and antioxidant defenses and decreased mitochondrial oxidative stress, medullary hypoxia, and renal injury. These findings implicate medullary mitochondrial damage in renal injury in experimental MetS, and position the mitochondria as a therapeutic target.
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Registered trials
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