An Update on Mechanistic Modes in AGEs Stimulated & ER and Inflammatory Stress-Modulated Control of the GLUT4 expression (SLC2A4 promoted) and Atherogenesis in Diabetes Mellitus-A Narrative Review

Earlier we had reviewed the role of herbal treatment, epigenetic modes, other mechanistic pathophysiological roles like macrophage polarization, epigenetics, role of adipokines &treatment using role of empagliflozin Extracellular Vesicles (ECV's), gut microbiota (GM) in Diabetes mellitus (DM) here we concentrated on more work on ER stress, inflammation, AGE's, Glut4 regulation by its gene. In the last 20 years complicated besides elegant pathways implicated in endoplasmic reticulum (ER) along with inflammatory stress reactions have been illustrated regarding taking part in the generation besides propagation of different diseases inclusive of Diabetes mellitus (DM). These pathways possess different actors taking part pointing to a complex crosstalk amongst ER along with inflammatory stress. Regarding DM, both ER and inflammatory stress are implicated in elimination of glycaemic regulation besides the generation of degenerative complications. Moreover, hyperglycemia enhanced the formation of advanced glycation end-products (AGE), that in turn further triggers the ER along with inflammatory stress, aiding in the inimical glycaemic homeostasis along with escalating the formation of DM complications. Here we conducted a narrative review utilizing search engines PubMed, Google Scholar; Web of Science; Embase; Cochrane review library utilizing the MeSH terms like AGEs; ER stress; inflammation) glucose transporter number 4(GLUT4); soluble carrier family 2 members 4(SLC2A4); glycaemic homeostasis; cardiovascular disease (CVD); atherogenesis from 1990-2022 till date. We found 300 articles out of which we used 130 articles for this review. Here we have highlighted role of AGEs-stimulated ER along with inflammatory stress in the control of GLUT4 expression besides atherogenesis in the form of commonest etiology regarding CVD generation, mortality along with morbidity in DM. Furthermore recently small molecule hampering