Abstract
The implications of lipid lowering drugs in the treatment of diabetic nephropathy have been considered. At the same time, the clinical efficacy of lipid lowering drugs has resulted in improvement in the cardiovascular functions of chronic kidney disease (CKD) patients with or without diabetes, but no remarkable improvement has been observed in the kidney outcome. Earlier lipid mediators have been shown to cause accumulative effects in diabetic nephropathy (DN). Here, we attempt to analyze the involvement of lipid mediators in DN. The hyperglycemia-induced overproduction of diacyglycerol (DAG) is one of the causes for the activation of protein kinase C (PKCs), which is responsible for the activation of pathways, including the production of VEGF, TGFβ1, PAI-1, NADPH oxidases, and NFҟB signaling, accelerating the development of DN. Additionally, current studies on the role of ceramide are one of the major fields of study in DN. Researchers have reported excessive ceramide formation in the pathobiological conditions of DN. There is less report on the effect of lipid lowering drugs on the reduction of PKC activation and ceramide synthesis. Regulating PKC activation and ceramide biosynthesis could be a protective measure in the therapeutic potential of DN. Lipid lowering drugs also upregulate anti-fibrotic microRNAs, which could hint at the effects of lipid lowering drugs in DN.
Highlights
Abnormalities in the lipoprotein metabolism are associated with patients with diabetic nephropathy (DN) [1]
Investigators in the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study [55] randomly allocated [56] 795 participants with type 2 diabetes mellitus to either fenofibrate (200 mg daily) or placebo, with a median follow-up period of 5 years
Clinical studies suggest that lipid lowering drugs improve the Conclusion The present review describes various aspects and implications of lipid lowering drugs in the treatment of DN
Summary
Abnormalities in the lipoprotein metabolism are associated with patients with diabetic nephropathy (DN) [1]. Statin treatment protects from the injuries caused by the DAG-Activated PKC activation in a variety of ways These pleotropic effects of statins include improvement in the endothelial function, reduction in the oxidative stress, reduction in the TGFβ1 level, decline in the level of inflammatory cytokines and sensitization of the Akt/PI3 kinase pathways, inducing the GLUT 4 translocation reviewed by Danesh and Kanwar [53]. Fenofibrate treatment reduced the total cardiovascular events (HR 0.89, 95% CI 0.80-0.99) [55] This benefit did not differ significantly between groups that had different eGFRs. In another report, the researchers summarized that fenofibrate should be considered as an additional therapeutic option, along with conventional risk-factor management, to further reduce CVD events and mortality and provide reno-protection to patients with diabetes and to those with moderate renal impairment [4].
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