Cholesterol synthesis inhibitors inhibit more than cholesterol synthesis.
The beneficial effects of HMG-CoA reductase inhibition in models of progressive glomerular injury may not all be due to reductions in circulating lipoproteins and decreases in glomerular lipoprotein deposition. Indeed, HMG-CoA reductase inhibitors may have direct effects on glomerular mesangial cells that could explain the amelioration of renal injury. Specifically, HMG-CoA reductase inhibitors block the synthesis of isoprenoids that are necessary for mesangial cell proliferation and other important cell functions. Thus, protein isoprenylation may play a critical role in the pathogenesis and treatment of lipid-induced glomerular injury.
Kasiske
B L
BL
Department of Medicine Hennepin County Medical Center, Minneapolis, Minnesota.
O'Donnell
M P
MP
Kim
Y
Y
Atluru
D
D
Keane
W F
WF
D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology*; D002455:Cell Division; D002633:Chemotaxis; D005920:Glomerular Mesangium / Q000166:cytology / Q000502:physiology; D006801:Humans; D006903:Hydroxymethylglutaryl CoA Reductases / Q000378:metabolism; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D017368:Protein Prenylation
D000924:Anticholesteremic Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D006903:Hydroxymethylglutaryl CoA Reductases