ArticleAmerican journal of nephrology2009
Reverse cholesterol transport pathway in experimental chronic renal failure.
Article in American journal of nephrology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 49 citations in OpenAlex.
- High-Density Lipoprotein in Patients with Diabetic Kidney Disease: Friend or Foe?International journal of molecular sciences · 2025Review
- Renoprotective Effect ofMolecules (Basel, Switzerland) · 2019Article
- High-density lipoprotein particle pattern and overall lipid responses to a short-term moderate-intensity aerobic exercise training intervention in patients with chronic kidney disease.Clinical kidney journal · 2017Article
- HDL Cholesterol Efflux Does Not Predict Cardiovascular Risk in Hemodialysis Patients.Journal of the American Society of Nephrology : JASN · 2017Article
- HDL abnormalities in nephrotic syndrome and chronic kidney disease.Nature reviews. Nephrology · 2016Review
- Role of dyslipidemia in impairment of energy metabolism, oxidative stress, inflammation and cardiovascular disease in chronic kidney disease.Clinical and experimental nephrology · 2014Review
- Metabolism, energetics, and lipid biology in the podocyte - cellular cholesterol-mediated glomerular injury.Frontiers in endocrinology · 2014Review
- Targeting the transcription factor Nrf2 to ameliorate oxidative stress and inflammation in chronic kidney disease.Kidney international · 2013Review
- Post-transcriptional nature of uremia-induced downregulation of hepatic apolipoprotein A-I production.Translational research : the journal of laboratory and clinical medicine · 2013Article
- Dysregulation of hepatic fatty acid metabolism in chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2013Article
- Reasons for the lack of salutary effects of cholesterol-lowering interventions in end-stage renal disease populations.Blood purification · 2013Review
- Statins in the management of dyslipidemia associated with chronic kidney disease.Nature reviews. Nephrology · 2012Review
- Salutary effects of hemodialysis on low-density lipoprotein proinflammatory and high-density lipoprotein anti-inflammatory properties in patient with end-stage renal disease.Journal of the National Medical Association · 2011Article
- Atherosclerosis in chronic kidney disease: the role of macrophages.Nature reviews. Nephrology · 2011Review
- HDL metabolism and activity in chronic kidney disease.Nature reviews. Nephrology · 2010Review
- An update on the lipid nephrotoxicity hypothesis.Nature reviews. Nephrology · 2009Review
- In vitro stimulation of HDL anti-inflammatory activity and inhibition of LDL pro-inflammatory activity in the plasma of patients with end-stage renal disease by an apoA-1 mimetic peptide.Kidney international · 2009Article
- Elevated serum cholesterol levels are associated with proteinuria over 0.5 g/day in premenopausal women with systemic lupus erythematosus.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundChronic renal failure (CRF) causes oxidative stress, inflammation, oxidation of lipoproteins, impaired maturation of HDL and accelerated atherosclerosis. Uptake of oxidized lipoproteins by macrophages via scavenger receptors (scavenger receptor class A type I--SR-AI, and lectin-like oxidized LDL receptor--LOX-1) leads to foam cell formation and atherosclerosis. HDL mitigates atherosclerosis by retrieving surplus cholesterol via ATP binding cassette transporter A1 (ABCA1) and ABCG1 transporters whose expression is regulated by liver X receptor (LXR). Free cholesterol reaching the surface of HDL is esterified by lecithin-cholesterol acyltransferase (LCAT) and sequestered in the core of HDL, thereby maximizing cholesterol uptake. In the liver, lipid-rich HDL unloads its lipid contents via reversible binding to SR-BI while lipid-poor HDL is degraded by the holo-receptor (ATP synthase beta-chain).
methodsExpression of the above molecules involved in reverse cholesterol/lipid transport was assessed in rats 8 weeks after 5/6 nephrectomy (CRF) or sham operation.
resultsCRF caused heavy accumulation of neutral lipids, upregulation of SR-AI, LOX-1, LXRalpha/beta, ABCA1 and ABCG1 in the aorta, reduction in LCAT in the plasma and no significant change in either SR-BI or beta-chain ATP synthase in the liver.
conclusionsLipid accumulation despite upregulation of the efflux (LXR, ABCA1, ABCG1) system in the aorta in CRF is largely due to upregulation of influx (SR-AI and LOX-1) pathway and LCAT deficiency.
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