ArticleKidney international2012
Deletion of scavenger receptor A protects mice from progressive nephropathy independent of lipid control during diet-induced hyperlipidemia.
Article in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Characterization of NLRP3 Inflammasome-Associated Hub Genes in the Progression of Diabetic Nephropathy.Immunity, inflammation and disease · 2026Article
- Protein Concentration Affects the Food Allergen γ-Conglutin Uptake and Bacteria-Induced Cytokine Production in Dendritic Cells.Biomolecules · 2023Article
- Redox regulation in diabetic kidney disease.American journal of physiology. Renal physiology · 2023Review
- IL-17C neutralization protects the kidney against acute injury and chronic injury.EBioMedicine · 2023Article
- Beneficial Effect of Kidney Bean Resistant Starch on Hyperlipidemia-Induced Acute Pancreatitis and Related Intestinal Barrier Damage in Rats.Molecules (Basel, Switzerland) · 2022Article
- M2 Macrophages as a Potential Target for Antiatherosclerosis Treatment.Neural plasticity · 2019Review
- High Glucose Promotes CD36 Expression by Upregulating Peroxisome Proliferator-Activated ReceptorBioMed research international · 2017Article
- Osteopontin deficiency reduces kidney damage from hypercholesterolemia in Apolipoprotein E-deficient mice.Scientific reports · 2016Article
- New molecular insights in diabetic nephropathy.International urology and nephrology · 2016Review
- Mitogen-activated protein kinase mediates mevalonate-stimulated human mesangial cell proliferation.Molecular medicine reports · 2015Article
- The evolving understanding of the contribution of lipid metabolism to diabetic kidney disease.Current diabetes reports · 2015Review
- Transcriptional patterns in peritoneal tissue of encapsulating peritoneal sclerosis, a complication of chronic peritoneal dialysis.PloS one · 2013Article
- A network-based approach for predicting Hsp27 knock-out targets in mouse skeletal muscles.Computational and structural biotechnology journal · 2013Article
- Fenofibrate attenuates renal lipotoxicity in uninephrectomized mice with high-fat diet-induced obesity.Jornal brasileiro de nefrologiaArticle
- ANGPTL3 in Podocytes Contributes to the Pathogenesis of Lupus Nephritis by Activating MSR1 in Macrophages.Kidney diseases (Basel, Switzerland)Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Scavenger receptor A (SR-A) is a key transmembrane receptor in the endocytosis of lipids and contributes to the pathogenesis of atherosclerosis. To assess its role in hyperlipidemic chronic kidney disease, wild-type and SR-A-deficient (knockout) mice underwent uninephrectomy followed by either normal or high-fat diet. After 16 weeks of diet intervention, hyperlipidemic wild-type mice presented characteristic features of progressive nephropathy: albuminuria, renal fibrosis, and overexpression of transforming growth factor (TGF)-β1/Smad. These changes were markedly diminished in hyperlipidemic knockout mice and attributed to reduced renal lipid retention, oxidative stress, and CD11c(+) cell infiltration. In vitro, overexpression of SR-A augmented monocyte chemoattractant protein-1 release and TGF-β1/Smad activation in HK-2 cells exposed to oxidized low-density lipoprotein. SR-A knockdown prevented lipid-induced cell injury. Moreover, wild-type to knockout bone marrow transplantation resulted in renal fibrosis in uninephrectomized mice following 16 weeks of the high-fat diet. In contrast, knockout to wild-type bone marrow transplantation led to markedly reduced albuminuria, CD11c(+) cell infiltration, and renal fibrosis compared to wild-type to SR-A knockout or wild-type to wild-type bone marrow transplanted mice, without difference in plasma lipid levels. Thus, SR-A on circulating leukocytes rather than resident renal cells predominantly mediates lipid-induced kidney injury.
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