Abstract
Diabetic nephropathy (DN) is one of the most common microvascular complications in diabetic patients; it is also an important cause of renal dysfunction, renal fibrosis, and end-stage renal disease. Unfortunately, the pathogenesis of DN is complex and has not yet been fully elucidated; hence, the pathogenesis of DN to determine effective treatments of crucial importance is deeply explored. Early DN research focuses on hemodynamic changes and metabolic disorders, and recent studies have shown the regulatory role of microRNAs (miRNAs) in genes, which may be a new diagnostic marker and therapeutic target for diabetic nephropathy. In this review, we summarize the recent advances in the clinical value and molecular mechanisms of miRNAs in DN, providing new ideas for the diagnosis and treatment of DN.
Highlights
Diabetic nephropathy (DN) is a progressive kidney disease secondary to diabetes and has been shown to be a major cause of end-stage renal disease (ESRD) [1], accounting for nearly 30%–50% of the world’s population requiring renal replacement therapy [2, 3]
The degree of renal fibrosis which was considered to be a key indicator of worsening kidney function is the core of DN high mortality [7], mainly due to the accumulation of extracellular matrix (ECM) proteins, as well as epithelial-to-mesenchymal transition (EMT) [8, 9]
Duan et al [44] showed that long noncoding RNA taurine-upregulated gene 1 can act as an endogenous miRNA sponge of miR-377, downregulating the expression level of miR-377, thereby attenuating the inhibition of its target gene peroxisome proliferator-activated receptor c (PPARc); PPARc is associated with mesangial cell proliferation, cell cycle, and glomerular ECM synthesis in diabetic environment [45]
Summary
Diabetic nephropathy (DN) is a progressive kidney disease secondary to diabetes and has been shown to be a major cause of end-stage renal disease (ESRD) [1], accounting for nearly 30%–50% of the world’s population requiring renal replacement therapy [2, 3]. DN is the result of a combination of factors, for example, genetic susceptibility, glucose metabolism disorder, renal hemodynamic changes, oxidative stress, and cytokines all play a very important role [4]. Appearance of microalbuminuria in patients with DN, with the progress of the disease, will cause significant proteinuria, impaired renal function, glomerular filtration rate (GFR) gradually decreased, eventually leading to ESRD [10]. Special miRNAs regulate the pathophysiology processes of DN by answering different signaling pathways and acting on different targets to inflammatory response, oxidative stress, immune response, fibrosis, and cell function
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