TY - JOUR
T1 - Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease
AU - Bajic, Vladan P.
AU - Van Neste, Christophe Marc
AU - Obradovic, Milan
AU - Zafirovic, Sonja
AU - Radak, Djordje
AU - Bajic, Vladimir B.
AU - Essack, Magbubah
AU - Isenovic, Esma R.
N1 - KAUST Repository Item: Exported on 2020-10-01
Acknowledged KAUST grant number(s): BAS/1/1606-01-01, FCC/1/1976-24-01
Acknowledgements: This work has been supported by grants from the Ministry of Education, Science and Technological Development, Republic of Serbia (No. 173033 (ERI), No. 173034 (BSP), and No. 41002 (DjR)). VBB has been supported by the King Abdullah University of Science and Technology (KAUST) Base Research Fund (BAS/1/1606-01-01) and ME by KAUST Office of Sponsored Research (OSR) Awards (No. FCC/1/1976-24-01).
PY - 2019/5/9
Y1 - 2019/5/9
N2 - More people die from cardiovascular diseases (CVD) than from any other cause. Cardiovascular complications are thought to arise from enhanced levels of free radicals causing impaired “redox homeostasis,” which represents the interplay between oxidative stress (OS) and reductive stress (RS). In this review, we compile several experimental research findings that show sustained shifts towards OS will alter the homeostatic redox mechanism to cause cardiovascular complications, as well as findings that show a prolonged antioxidant state or RS can similarly lead to such cardiovascular complications. This experimental evidence is specifically focused on the role of glutathione, the most abundant antioxidant in the heart, in a redox homeostatic mechanism that has been shifted towards OS or RS. This may lead to impairment of cellular signaling mechanisms and elevated pools of proteotoxicity associated with cardiac dysfunction.
AB - More people die from cardiovascular diseases (CVD) than from any other cause. Cardiovascular complications are thought to arise from enhanced levels of free radicals causing impaired “redox homeostasis,” which represents the interplay between oxidative stress (OS) and reductive stress (RS). In this review, we compile several experimental research findings that show sustained shifts towards OS will alter the homeostatic redox mechanism to cause cardiovascular complications, as well as findings that show a prolonged antioxidant state or RS can similarly lead to such cardiovascular complications. This experimental evidence is specifically focused on the role of glutathione, the most abundant antioxidant in the heart, in a redox homeostatic mechanism that has been shifted towards OS or RS. This may lead to impairment of cellular signaling mechanisms and elevated pools of proteotoxicity associated with cardiac dysfunction.
UR - http://hdl.handle.net/10754/652879
UR - https://www.hindawi.com/journals/omcl/2019/5028181/
UR - http://www.scopus.com/inward/record.url?scp=85068390274&partnerID=8YFLogxK
U2 - 10.1155/2019/5028181
DO - 10.1155/2019/5028181
M3 - Article
C2 - 31210841
SN - 1942-0900
VL - 2019
SP - 1
EP - 14
JO - Oxidative medicine and cellular longevity
JF - Oxidative medicine and cellular longevity
ER -
