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.