Pharmacological Protection against Ischemia-Reperfusion Injury by Regulating the Nrf2-Keap1-ARE Signaling Pathway

Ucar, Bercis Imge and Ucar, Gulberk and Saha, Sarmistha and Buttari, Brigitta and Profumo, Elisabetta and Saso, Luciano (2021) Pharmacological Protection against Ischemia-Reperfusion Injury by Regulating the Nrf2-Keap1-ARE Signaling Pathway. Antioxidants, 10 (6). p. 823. ISSN 2076-3921

[thumbnail of antioxidants-10-00823.pdf] Text
antioxidants-10-00823.pdf - Published Version

Download (941kB)

Abstract

Ischemia/reperfusion (I/R) injury is associated with substantial clinical implications, including a wide range of organs such as the brain, kidneys, lungs, heart, and many others. I/R injury (IRI) occurs due to the tissue injury following the reestablishment of blood supply to ischemic tissues, leading to enhanced aseptic inflammation and stimulation of oxidative stress via reactive oxygen and nitrogen species (ROS/RNS). Since ROS causes membrane lipids’ peroxidation, triggers loss of membrane integrity, denaturation of proteins, DNA damage, and cell death, oxidative stress plays a critical part in I/R pathogenesis. Therefore, ROS regulation could be a promising therapeutic strategy for IRI. In this context, Nrf2 (NF-E2-related factor 2) is a transcription factor that regulates the expression of several factors involved in the cellular defense against oxidative stress and inflammation, including heme oxygenase-1 (HO-1). Numerous studies have shown the potential role of the Nrf2/HO-1 pathway in IRI; thus, we will review the molecular aspects of Nrf2/Kelch-like ECH-associated protein 1 (Keap1)/antioxidant response element (ARE) signaling pathway in I/R, and we will also highlight the recent insights into targeting this pathway as a promising therapeutic strategy for preventing IRI.

Item Type: Article
Subjects: ScienceOpen Library > Biological Science
Depositing User: Managing Editor
Date Deposited: 29 Sep 2023 12:28
Last Modified: 26 Jul 2024 06:48
URI: http://scholar.researcherseuropeans.com/id/eprint/1881

Actions (login required)

View Item
View Item