scholarly journals Gene expression of LDL receptor, HMG-CoA reductase, and cholesterol-7 alpha-hydroxylase in chronic renal failure

1997 ◽  
Vol 12 (7) ◽  
pp. 1381-1386 ◽  
Author(s):  
K. Liang ◽  
N. D. Vaziri
Keyword(s):  
Gene Expression ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Ldl Receptor ◽  
Hmg Coa Reductase ◽  
Coa Reductase

Contribution of increased HMG-CoA reductase gene expression to hypercholesterolemia in experimental chronic renal failure

2003 ◽  
pp. 187-191
Author(s):  
Michal Chmielewski ◽  
Elzbieta Sucajtys ◽  
Julian Swierczynski ◽  
Boleslaw Rutkowski ◽  
Wojciech Bogusławski
Keyword(s):  
Gene Expression ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Hmg Coa Reductase ◽  
Reductase Gene ◽  
Coa Reductase

Effects of ezetimibe and/or simvastatin on LDL receptor protein expression and on LDL receptor and HMG-CoA reductase gene expression: A randomized trial in healthy men

2008 ◽  
Vol 198 (1) ◽  
pp. 198-207 ◽  
Author(s):  
Ioanna Gouni-Berthold ◽  
Heiner K. Berthold ◽  
Helena Gylling ◽  
Maarit Hallikainen ◽  
Eleni Giannakidou ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Expression ◽  
Randomized Trial ◽  
Ldl Receptor ◽  
Receptor Protein ◽  
Hmg Coa Reductase ◽  
Healthy Men ◽  
Reductase Gene ◽  
Coa Reductase

HMG-CoA reductase inhibition reverses LCAT and LDL receptor deficiencies and improves HDL in rats with chronic renal failure

2005 ◽  
Vol 288 (3) ◽  
pp. F539-F544 ◽  
Author(s):  
K. Liang ◽  
C. H. Kim ◽  
N. D. Vaziri
Keyword(s):  
Renal Failure ◽  
Total Cholesterol ◽  
Reductase Activity ◽  
Plasma Cholesterol ◽  
Ldl Receptor ◽  
Hdl Cholesterol ◽  
Hmg Coa Reductase ◽  
Cholesterol Ratio ◽  
Plasma Lcat ◽  
Coa Reductase

Dyslipidemia is a prominent feature of chronic renal failure (CRF) and a major risk factor for atherosclerosis and the progression of renal disease. CRF-induced dyslipidemia is marked by hypertriglyceridemia and a shift in plasma cholesterol from HDL to the ApoB-containing lipoproteins. Several studies have demonstrated a favorable response to administration of 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitors (statins) in CRF. This study was intended to explore the effect of statin therapy on key enzymes and receptors involved in cholesterol metabolism. Accordingly, CRF ( nephrectomized) and sham-operated rats were randomized to untreated and statin-treated (rosuvastatin 20 mg·kg−1·day−1) groups and observed for 6 wk. The untreated CRF rats exhibited increased total cholesterol-to-HDL cholesterol ratio, diminished plasma lecithin:cholesterol acyltransferase (LCAT) and the hepatic LDL receptor, elevated hepatic acyl-CoA:cholesterol acyltransferase (ACAT), and no change in hepatic HMG-CoA reductase, cholesterol 7α-hydroxylase, or HDL receptor (SRB-1). Statin administration lowered HMG-CoA reductase activity, normalized plasma LCAT, total cholesterol-to-HDL cholesterol ratio, and hepatic LDL receptor but did not significantly change either plasma total cholesterol, hepatic cholesterol 7α-hydroxylase, total ACAT activity, or SRB-1 in the CRF animals. Statin administration to the normal control rats led to significant increases in plasma LCAT and hepatic LDL receptor, significant reductions of total cholesterol-to-HDL cholesterol ratio, hepatic HMG-CoA reductase activity, and cholesterol 7α-hydroxylase abundance with virtually no change in plasma cholesterol concentration. Thus administration of rosuvastatin reversed LCAT and LDL receptor deficiencies and promoted a shift in plasma cholesterol from ApoB-containing lipoproteins to HDL in CRF rats.

Glycation and HMG-CoA Reductase Inhibitors: Implication in Diabetes and Associated Complications

2019 ◽  
Vol 15 (3) ◽  
pp. 213-223 ◽  
Author(s):  
Rabia Nabi ◽  
Sahir Sultan Alvi ◽  
Mohd. Saeed ◽  
Saheem Ahmad ◽  
Mohammad Salman Khan
Keyword(s):  
Oxidized Ldl ◽  
Advanced Glycation Endproducts ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Protective Role ◽  
Therapeutic Effects ◽  
Hmg Coa Reductase ◽  
Toxicological Effects ◽  
Coa Reductase

Introduction: Diabetes Mellitus (DM) acts as an absolute mediator of cardiovascular risk, prompting the prolonged occurrence, size and intricacy of atherosclerotic plaques via enhanced Advanced Glycation Endproducts (AGEs) formation. Moreover, hyperglycemia is associated with enhanced glyco-oxidized and oxidized Low-Density Lipoprotein (LDL) possessing greater atherogenicity and decreased the ability to regulate HMG-CoA reductase (HMG-R). Although aminoguanidine (AG) prevents the AGE-induced protein cross-linking due to its anti-glycation potential, it exerts several unusual pharmaco-toxicological effects thus restraining its desirable therapeutic effects. HMG-R inhibitors/statins exhibit a variety of beneficial impacts in addition to the cholesterol-lowering effects. Objective: Inhibition of AGEs interaction with receptor for AGEs (RAGE) and glyco-oxidized-LDL by HMG-R inhibitors could decrease LDL uptake by LDL-receptor (LDL-R), regulate cholesterol synthesis via HMG-R, decrease oxidative and inflammatory stress to improve the diabetes-associated complications. Conclusion: Current article appraises the pathological AGE-RAGE concerns in diabetes and its associated complications, mainly focusing on the phenomenon of both circulatory AGEs and those accumulating in tissues in diabetic nephropathy, diabetic neuropathy, and diabetic retinopathy, discussing the potential protective role of HMG-R inhibitors against diabetic complications.

In Vivo LDL Receptor and HMG-CoA Reductase Regulation in Human Lymphocytes and Its Alterations During Aging

1995 ◽  
Vol 15 (7) ◽  
pp. 872-878 ◽  
Author(s):  
Thomas M. Stulnig ◽  
Helmut Klocker ◽  
H. James Harwood ◽  
Günther Jürgens ◽  
Dieter Schönitzer ◽  
...  
Keyword(s):  
Human Lymphocytes ◽  
Ldl Receptor ◽  
Hmg Coa Reductase ◽  
Coa Reductase
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