The Role of Autophagy in Type 2 Diabetic Kidney Disease Management

Abstract

Diabetic kidney disease (DKD), or diabetic nephropathy (DN), is one of the most prevalent complications of type 2 diabetes mellitus (T2DM) and causes severe burden on the general welfare of T2DM patients around the world. While several new agents have shown promise in treating this condition and potentially halting the progression of the disease, more work is needed to understand the complex regulatory network involved in the disorder. Recent studies have provided new insights into the connection between autophagy, a physiological metabolic process known to maintain cellular homeostasis, and the pathophysiological pathways of DKD. Typically, autophagic activity plays a role in DKD progression mainly by promoting an inflammatory response to tissue damage, while both overactivated and downregulated autophagy worsen disease outcomes in different stages of DKD. This correlation demonstrates the potential of autophagy as a novel therapeutic target for the disease, and also highlights new possibilities for utilizing already available DN-related medications. In this review, we summarize findings on the relationship between autophagy and DKD, and the impact of these results on clinical management strategies.

Exosomes derived from mesenchymal stem cells in diabetes and diabetic complications

“…The activation of mTOR was crucial to the preservation of glomerular podocyte function, as well as the occurrence of glomerular and tubular cell hypertrophy and podocytes damage, on the contrary, mTOR inhibition might preserve podocytes and prevent the progression of diabetic nephropathy [ 70 ]. Impairment of autophagy leads to the cumulation of collagen in extracellular matrix, dysfunction of mitochondria in podocytes, and elevated levels of ER stress in tubular cells [ 71 ]. BMSCs-derived exosomes could ameliorate renal function as well as promote repairation of renal tissues by the regulation of autophagy via inhibiting the mTOR signaling pathway, suppressing TGF-β expression, and reducing fibrosis in diabetic rats [ 72 ].…”