Regulation, Pathological Role, and Therapeutic Potential of Endoplasmic Reticulum Stress in Diabetic Nephrology

Author(s): Amy Sears*

Understanding the functions and processes of endoplasmic reticulum (ER) stress in the onset and progression of diabetic nephropathy has advanced recently (DN). Renal cells experience ER stress and apoptosis as a result of hyperglycemia. ER stress can be either cytotoxic or cytoprotective when it is induced. Animals given an experimental dose of ER stress inhibitors experienced lessened kidney damage. In light of these results, pharmacological treatments that normalise ER stress represent a promising strategy to halt or stop the course of DN. The causes, functions, and therapeutic implications of these findings are reviewed in the current article. The cardiovascular disorders related to atherosclerosis and endoplasmic reticulum (ER) stress are intimately related (CVDs). It happens as a result of a variety of pathogenic events that disrupt ER homeostasis, generating an accumulation of unfolded or misfolded proteins in the ER lumen and culminating in ER malfunction. Here, we talk about how ER stress affects several cell types in atherosclerotic plaques. This discussion covers common atherosclerosis-related ER stressors in various lesional cells, which all contribute to the clinical progression of atherosclerosis, as well as the activation of apoptotic and inflammatory pathways induced by prolonged ER stress, particularly in advanced lesional macrophages and endothelial cells (ECs). Targeting these processes to lessen ER stress may be a novel treatment approach given the significance of ER stress and the unfolded protein response (UPR) signalling pathways in atherosclerosis and CVDs.