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Genetic and Kidney Cyst Diseases / Dialysis and Renal Disease Management · Journal article
Acta Physiologica · September 7, 2026
Encouraging direction, but not yet definitive.
This preclinical study demonstrates that aerobic exercise ameliorates high-fat diet–induced renal injury in mice through suppression of the Drp1-mtROS pathway, with corroborating evidence from pharmacological inhibition and genetic knockdown. The mechanism is novel and internally consistent across model systems, but the lack of human data, unblinded design, and reliance on surrogate endpoints limit immediate clinical applicability.
Experimental study combining in vivo mouse model with in vitro cell-based mechanistic validation. High-fat diet–fed mice (species and age not specified); HK-2 immortalized human renal proximal tubule cells treated with palmitic acid.. Intervention: Aerobic exercise for 8 weeks; intraperitoneal Drp1 inhibitor (Mdivi-1); Drp1 knockdown via transfection in HK-2 cells.. Compared with: High-fat diet–fed control mice (exercise not specified for control group); non-transfected palmitic acid–treated HK-2 cells..
Aerobic exercise reduced serum creatinine and blood urea nitrogen in HFD-fed mice Exercise suppressed Drp1 phosphorylation at Ser616 and reduced renal mtROS production Mdivi-1 (Drp1 inhibitor) reproduced metabolic, mitochondrial, and renoprotective effects of exercise
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This work identifies a potential mechanistic target (Drp1-mtROS pathway) for exercise-based nephroprotection in obesity-related kidney disease. However, confirmation in human studies and evaluation of hard renal endpoints are needed before clinical translation.
A mechanistic study in mice and cultured cells demonstrating aerobic exercise reduces renal injury via Drp1-mtROS inhibition; the pathway is novel and supported by consistent findings across models, but lacks direct clinical validation and hard renal outcomes.
As stated by the source record.
Quoted from the source exactly as published.
This work identifies a potential mechanistic target (Drp1-mtROS pathway) for exercise-based nephroprotection in obesity-related kidney disease. However, confirmation in human studies and evaluation of hard renal endpoints are needed before clinical translation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
AIM: Aberrant activation of dynamin-related protein 1 (Drp1) promotes excessive mitochondrial reactive oxygen species (mtROS) production; however, whether the Drp1-mtROS pathway mediates the renoprotective effects of aerobic exercise remains unclear. METHODS: High-fat diet (HFD)-fed mice were subjected to aerobic exercise or were intraperitoneally injected with the Drp1 inhibitor Mdivi-1 for 8 weeks. Fat mass, serum biochemical parameters, renal histopathology, mtROS production, oxidative stress-related markers, mitochondrial ultrastructure, mitochondrial membrane potential, ATP content, and protein expression were assessed. In parallel, Drp1 was knocked down in palmitic acid (PA)-treated HK-2 cells to further evaluate the role of the Drp1-mtROS pathway in lipid overload-induced renal tubular cell injury. RESULTS: Aerobic exercise reduced body weight and fat mass, improved circulating lipid profiles, and decreased serum creatinine and blood urea nitrogen levels in HFD-fed mice. Exercise also alleviated renal tubular injury, mesangial expansion, interstitial fibrosis, podocyte foot process effacement, and renal lipid accumulation. Mechanistically, aerobic exercise suppressed Drp1 phosphorylation at Ser616, reduced renal mtROS production and oxidative stress, improved mitochondrial morphology, restored mitochondrial membrane potential and ATP production, and modulated the expression of lipid-metabolism-related proteins. Pharmacological inhibition of Drp1 with Mdivi-1 largely reproduced the metabolic, mitochondrial, and renoprotective effects of aerobic exercise. Furthermore, Drp1 knockdown attenuated PA-induced mtROS accumulation, oxidative stress, mitochondrial dysfunction, and lipid deposition in HK-2 cells. CONCLUSION: Aerobic exercise exerts a protective effect on the kidneys of HFD-fed mice, at least in part, by inhibiting the Drp1-mtROS pathway. This provides insights into the benefits of aerobic exercise in obesity-related nephropathy.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.