A Novel Biomarker MicroRNA-92a-3p as a Link between Cardiovascular Disease and Chronic Kidney Disease | Abstract
Journal of Carcinogenesis & Mutagenesis

Journal of Carcinogenesis & Mutagenesis
Open Access

ISSN: 2157-2518


A Novel Biomarker MicroRNA-92a-3p as a Link between Cardiovascular Disease and Chronic Kidney Disease

Kazumi Fujioka*

The emergence of microRNAs (miRNA) as significant regulators of pathophysiological processes has provided new therapeutic strategies in atherosclerotic status. Recently, the author has described that microRNA-92a-3p (miR-92a-3p), having pleiotropic manner is a potential therapeutic target in atherosclerosis-related diseases. The author has previously described that mild renal dysfunction was associated with endothelial dysfunction in women and that the cardio-renal interrelationship may be also suggested under mild renal dysfunction. Shang et al. suggested mcroiRNA-92a (miR-92a) as a crucial link between chronic kidney disease (CKD) and cardiovascular disease (CVD) by mediating uremia-impaired endothelial dysfunction. On the evidences of relationships between miR-92a and flowmediated vasodilation (FMD) and between miR-92a and estimated glomerular filtration rate (eGFR) level, the author indicates that miR-92a gene expression profile in endothelial cell and the circulating level reflecting FMD study and eGFR level which were established indicators may be an early diagnostic biomarker in atherosclerosis-related CKD, having a link between CVD and CKD. Shang et al. also indicated miR-92a as a link among CKD-induced uremia, oxidative stress, and endothelial dysfunction. On the proof of the interrelationship among miR-92a profile, FMD study, and eGFR level, the author suggests that atherosclerosis-related CKD cause oxidative stress, leading to miR-92a expression, endothelial dysfunction, and renal dysfunction. In CKD with advanced stage, oxidative stress derived from uremic toxin mainly contributes to miR-92a gene expression profile, endothelial dysfunction, and renal failure. Wiese et al. showed that renal injury significantly increased endothelial miR-92a-3p and dual inhibition of miR-92a-3p and miR-489-3p significantly reduced atherosclerotic lesion compared to control, thereby, suggesting that miR-92a-3p and/or miR-489-3p are potential therapeutic targets in atherosclerosis-related CKD. The author emphasizes that clinically and genetically, the studies have provided a link between CVD and CKD mediated by endothelial dysfunction even at early stage.

Published Date: 2020-04-24; Received Date: 2020-02-24