ArticleThe American journal of pathology2003
Acute tubular injury causes dysregulation of cellular cholesterol transport proteins.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Metabolic effects of RUBCN/Rubicon deficiency in kidney proximal tubular epithelial cells.Autophagy · 2020Article
- Intrarenal arteriosclerosis and telomere attrition associate with dysregulation of the cholesterol pathway.Aging · 2020Article
- The role of CD47 in pathogenesis and treatment of renal ischemia reperfusion injury.Pediatric nephrology (Berlin, Germany) · 2019Review
- Anthocyanins inhibit high-glucose-induced cholesterol accumulation and inflammation by activating LXRα pathway in HK-2 cells.Drug design, development and therapy · 2015Article
- Article
- 'Biologic memory' in response to acute kidney injury: cytoresistance, toll-like receptor hyper-responsiveness and the onset of progressive renal disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2013Review
- Acute unilateral ischemic renal injury induces progressive renal inflammation, lipid accumulation, histone modification, and "end-stage" kidney disease.American journal of physiology. Renal physiology · 2011Article
- Chimeric maternal cells in offspring do not respond to renal injury, inflammatory or repair signals.Chimerism · 2011Article
- Native LDL-induced oxidative stress in human proximal tubular cells: multiple players involved.Journal of cellular and molecular medicine · 2011Article
- Atherosclerosis in chronic kidney disease: the role of macrophages.Nature reviews. Nephrology · 2011Review
- High-calorie diet partially ameliorates dysregulation of intrarenal lipid metabolism in remnant kidney.The Journal of nutritional biochemistry · 2010Article
- HDL metabolism and activity in chronic kidney disease.Nature reviews. Nephrology · 2010Review
- Steroidogenic acute regulatory-related lipid transfer domain protein 5 localization and regulation in renal tubules.American journal of physiology. Renal physiology · 2009Article
- Renal mass reduction results in accumulation of lipids and dysregulation of lipid regulatory proteins in the remnant kidney.American journal of physiology. Renal physiology · 2009Article
- Growth and development alter susceptibility to acute renal injury.Kidney international · 2008Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Acute renal injury causes accumulation of free and esterified cholesterol (FC, CE) in proximal tubules, mediated, at least in part, by increased cholesterol synthesis. Normally, this would trigger compensatory mechanisms such as increased efflux and decreased influx to limit or reverse the cholesterol overload state. This study sought to determine the integrity of these compensatory pathways following acute renal damage. Rhabdomyolysis-induced acute renal failure was induced in mice by glycerol injection. Normal mice served as controls. After 18 hours, BUN levels and renal cortical FC/CE content were determined. Expression of ABCA-1 and SR-B1 (cholesterol efflux proteins) were assessed by Western blot. Renal cortical LDL receptor (LDL-R; a cholesterol importer) regulation was gauged by quantifying its mRNA. To obtain proximal tubule cell-specific data, the impact of oxidant (Fe) stress on cultured HK-2 cell LDL-R, SR-B1, and ABCA-1 proteins and their mRNAs (versus controls) was assessed. Glycerol evoked marked azotemia and striking FC/CE increments (44%, 384%, respectively). Paradoxically, renal cortical SR-B1 and ABCA-1 protein reductions and LDL-R mRNA increments resulted. Fe-induced injury suppressed HK-2 cell SR-B1, ABCA-1, and their mRNAs. LDL-R protein rose with the in vitro Fe challenge. Renal tubular cell injury causes dysregulation of SR-B1, ABCA-1, and LDL-R protein expression, changes which should contribute to a cholesterol overload state. Reductions in HK-2 cell SR-B1 and ABCA-1 mRNAs and increases in renal cortical LDL-R mRNA imply that this dysregulation reflects, at least in part, altered genomic/transcriptional events.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.