Oxidative stress in the pathophysiology of type 2 diabetes and related complications: Current therapeutics strategies and future perspectives

Simple item page
dc.contributor.authorBhatti, Jasvinder Singh
dc.contributor.authorSehrawat, Abhishek
dc.contributor.authorMishra, Jayapriya
dc.contributor.authorSidhu, Inderpal Singh
dc.contributor.authorNavik, Umashanker
dc.contributor.authorKhullar, Naina
dc.contributor.authorKumar, Shashank
dc.contributor.authorBhatti, Gurjit Kaur
dc.contributor.authorReddy, P. Hemachandra
dc.date.accessioned2024-01-21T10:54:05Z
dc.date.accessioned2024-08-14T07:40:51Z
dc.date.available2024-01-21T10:54:05Z
dc.date.available2024-08-14T07:40:51Z
dc.date.issued2022-04-07T00:00:00
dc.description.abstractType 2 diabetes (T2DM) is a persistent metabolic disorder rising rapidly worldwide. It is characterized by pancreatic insulin resistance and ?-cell dysfunction. Hyperglycemia induced reactive oxygen species (ROS) production and oxidative stress are correlated with the pathogenesis and progression of this metabolic disease. To counteract the harmful effects of ROS, endogenous antioxidants of the body or exogenous antioxidants neutralise it and maintain bodily homeostasis. Under hyperglycemic conditions, the imbalance between the cellular antioxidant system and ROS production results in oxidative stress, which subsequently results in the development of diabetes. These ROS are produced in the endoplasmic reticulum, phagocytic cells and peroxisomes, with the mitochondrial electron transport chain (ETC) playing a pivotal role. The exacerbated ROS production can directly cause structural and functional modifications in proteins, lipids and nucleic acids. It also modulates several intracellular signaling pathways that lead to insulin resistance and impairment of ?-cell function. In addition, the hyperglycemia-induced ROS production contributes to micro- and macro-vascular diabetic complications. Various in-vivo and in-vitro studies have demonstrated the anti-oxidative effects of natural products and their derived bioactive compounds. However, there is conflicting clinical evidence on the beneficial effects of these antioxidant therapies in diabetes prevention. This review article focused on the multifaceted role of oxidative stress caused by ROS overproduction in diabetes and related complications and possible antioxidative therapeutic strategies targeting ROS in this disease. � 2022 Elsevier Inc.en_US
dc.identifier.doi10.1016/j.freeradbiomed.2022.03.019
dc.identifier.issn8915849
dc.identifier.urihttp://10.2.3.109/handle/32116/4209
dc.identifier.urlhttps://linkinghub.elsevier.com/retrieve/pii/S0891584922001228
dc.language.isoen_USen_US
dc.publisherElsevier Inc.en_US
dc.subjectAntioxidant enzymesen_US
dc.subjectElectron transport systemen_US
dc.subjectHyperglycemiaen_US
dc.subjectInsulin resistanceen_US
dc.subjectOxidative stressen_US
dc.subjectPancreatic ?-cellsen_US
dc.subjectReactive oxygen speciesen_US
dc.titleOxidative stress in the pathophysiology of type 2 diabetes and related complications: Current therapeutics strategies and future perspectivesen_US
dc.title.journalFree Radical Biology and Medicineen_US
dc.typeReviewen_US
dc.type.accesstypeOpen Accessen_US

Files

Collections

Human Genetics And Molecular Medicine - Research Publications