ArticleCell death & disease2020
High-fat diet promotes renal injury by inducing oxidative stress and mitochondrial dysfunction.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers.
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Who cites it
173 citing papers in PubMed, 310 citations in OpenAlex.
- The Role of Bariatric Surgery in Kidney Disease: Evidence, Controversies, and Future Needs.Obesity surgery · 2026Review
- Aerobic Exercise Ameliorates Renal Injury in High-Fat Diet-Fed Mice: A Novel Effect Mediated by the Drp1-mtROS Pathway.Acta physiologica (Oxford, England) · 2026Article
- Urotensin II Receptor Deletion Mitigates Kidney Injury and Renal Lipid Remodeling in Mice Fed a Long-Term High-Fat Diet.FASEB bioAdvances · 2026Article
- Beyond eGFR and Albuminuria: Biological Pathways and Multiomics in Cardiovascular-Kidney-Metabolic Disease.Kidney international reports · 2026Review
- Dose-Dependent Anti-Obesity and Protective Effects of Chia (Food science & nutrition · 2026Article
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- Association of remnant cholesterol with long-term outcomes in kidney transplant recipients: a retrospective cohort study.Lipids in health and disease · 2026Article
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- Irisin-Driven AMPK-PGC-1α Activation Underlies the Renoprotective Effects of Swimming Exercise in Obesity-Induced Kidney Injury.Biomolecules · 2026Article
- Three-dimensional interactive network: Mitochondrial-metabolic-calcium homeostasis driving Alzheimer's disease.Genes & diseases · 2026Review
- Effects of NAD⁺ repletion with Nicotinamide riboside on obesity-induced chronic kidney disease and renal cell lipotoxicity.Scientific reports · 2026Article
- Metabolic dysfunction-associated steatotic liver disease and steatohepatitis-associated hepatocarcinoma preclinical models.Nature reviews. Gastroenterology & hepatology · 2026Review
- Collagen-specific molecular chaperone Hsp47 in inguinal white adipose tissue promotes high-fat diet-induced inflammatory gene expression in male mice.Scientific reports · 2026Article
- Shikonin alleviates high-fat diet-induced vascular aging and dysfunction by inhibiting oxidative stress and mitochondrial damage.Molecular biology reports · 2026Article
- A High-fat, High-salt Diet Model of MDAKD Impairs Bioenergetic Efficiency for ATP Synthesis.bioRxiv : the preprint server for biology · 2026Article
- Time-of-Day Defines the Risk of Thermally Abused Frying Oil to Renal Injury by Modulating the Diurnal Dynamics of Oxylipins.Exploration (Beijing, China) · 2026Article
- Context-Dependent Roles of ANGPTL2-Mediated Inflammaging in Tissue Homeostasis, Pathological Tissue Remodeling, and Longevity.Aging cell · 2026Article
- Dietary lecithin attenuates adverse effects of high fat diet on antioxidant activity, inflammation and fibrotic damage in the kidney of blunt snout bream (Megalobrama amblycephala).Fish physiology and biochemistry · 2026Article
- A High Fat/High Sucrose Diet Alters the Skeletal Response to Adenine-Induced Chronic Kidney Disease in Male Rats.Calcified tissue international · 2026Article
113 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity has been recognized as a major risk factor for chronic kidney disease, but the underlying mechanism remains elusive. Here, we investigated the mechanism whereby long-term high-fat diet (HFD) feeding induces renal injury in mice. The C57BL/6 mice fed HFD for 16 weeks developed obesity, diabetes, and kidney dysfunction manifested by albuminuria and blood accumulation of BUN and creatinine. The HFD-fed kidney showed marked glomerular and tubular injuries, including prominent defects in the glomerular filtration barrier and increased tubular cell apoptosis. Mechanistically, HFD feeding markedly increased triglyceride and cholesterol contents in the kidney and activated lipogenic pathways for cholesterol and triglyceride synthesis. HFD feeding also increased oxidative stress and induced mitochondrial fission in tubular cells, thereby activating the pro-apoptotic pathway. In HK-2 and mesangial cell cultures, high glucose, fatty acid, and TNF-α combination was able to activate the lipogenic pathways, increase oxidative stress, promote mitochondrial fission, and activate the pro-apoptotic pathway, all of which could be attenuated by an inhibitor that depleted reactive oxygen species. Taken together, these observations suggest that long-term HFD feeding causes kidney injury at least in part as a result of tissue lipid accumulation, increased oxidative stress, and mitochondrial dysfunction, which promote excess programmed cell death.
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