ArticleKidney research and clinical practice2018
Human CD36 overexpression in renal tubules accelerates the progression of renal diseases in a mouse model of folic acid-induced acute kidney injury.
Article in Kidney research and clinical practice, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Abnormal lipid metabolism in senescent renal tubular cells in diabetic nephropathy.Cellular and molecular life sciences : CMLS · 2026Review
- Citronellol protects renal function by exerting anti-inflammatory and antiapoptotic effects against acute kidney injury induced by folic acid in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Sulforaphane Restores Mitochondrial β-Oxidation and Reduces Renal Lipid Accumulation in a Model of Releasing Unilateral Ureteral Obstruction.Antioxidants (Basel, Switzerland) · 2025Article
- Acute kidney injury through a metabolic lens: pathological reprogramming mechanisms and clinical translation potential.Frontiers in physiology · 2025Review
- Does the Composition of Gut Microbiota Affect Chronic Kidney Disease? Molecular Mechanisms Contributed to Decreasing Glomerular Filtration Rate.International journal of molecular sciences · 2024Review
- CD36 promotes tubular ferroptosis by regulating the ubiquitination of FSP1 in acute kidney injury.Genes & diseases · 2024Article
- A novel method for automated crystal visualization and quantification in murine folic acid-induced acute kidney injury.American journal of physiology. Renal physiology · 2024Article
- Increased renal uptake and urine excretion of oxidized LDL is possibly associated with formation of large calcium oxalate nephrolithiasis: a preliminary study.World journal of urology · 2023Article
- Sulforaphane Protects against Unilateral Ureteral Obstruction-Induced Renal Damage in Rats by Alleviating Mitochondrial and Lipid Metabolism Impairment.Antioxidants (Basel, Switzerland) · 2022Article
- Fatty Acid β-Oxidation in Kidney Diseases: Perspectives on Pathophysiological Mechanisms and Therapeutic Opportunities.Frontiers in pharmacology · 2022Review
- Folic acid-induced animal model of kidney disease.Animal models and experimental medicine · 2021Review
- PGC-1α, a potential therapeutic target against kidney aging.Aging cell · 2019Review
- The Effect of Overexpression of the Enhancer of Zeste Homolog 1 (EZH1) Gene on Aristolochic Acid-Induced Injury in HK-2 Human Kidney Proximal Tubule Cells In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Multiparametric MRI detects longitudinal evolution of folic acid-induced nephropathy in mice.American journal of physiology. Renal physiology · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute kidney injury (AKI) is a risk factor for progression to chronic kidney disease, with even subclinical AKI episodes progressing to chronic kidney disease. Several risk factors such as preexisting kidney disease, hyperglycemia, and hypertension may aggravate renal disease after AKI. However, mechanisms underlying the progression of AKI are still unclear. This study identified the effect of human cluster of differentiation 36 (CD36) overexpression on the progression of folic acid-induced AKI.
methodsPax8-rtTA/tetracycline response element-human CD36 transgenic mice were used to elucidate the effect of human CD36 overexpression in the proximal tubules on folic acid-induced AKI.
resultsResults of histological analysis showed severely dilated tubules with casts and albuminuria in folic acid-treated transgenic mice overexpressing human CD36 compared with folic acid-treated wild-type mice. In addition, analysis of mRNA expression showed a significant increase in the
conclusionHuman CD36-overexpressing transgenic mice showed severe pathological changes and albuminuria compared with wild-type mice. Moreover, mRNA expression of the collagen 3a1 gene increased in folic acid-treated transgenic mice. These results suggest that human CD36 overexpression is a risk factor of AKI and its progression to chronic kidney disease.
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