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Uncoupling proteins in the mitochondrial defense against oxidative stress.
Prog Retin Eye Res. 2021 Jul; 83:100941.PR

Abstract

Oxidative stress is a major component of most major retinal diseases. Many extrinsic anti-oxidative strategies have been insufficient at counteracting one of the predominant intrinsic sources of reactive oxygen species (ROS), mitochondria. The proton gradient across the inner mitochondrial membrane is a key driving force for mitochondrial ROS production, and this gradient can be modulated by members of the mitochondrial uncoupling protein (UCP) family. Of the UCPs, UCP2 shows a widespread distribution and has been shown to uncouple oxidative phosphorylation, with concomitant decreases in ROS production. Genetic studies using transgenic and knockout mice have documented the ability of increased UCP2 activity to provide neuroprotection in models of a number of diseases, including retinal diseases, indicating that it is a strong candidate for a therapeutic target. Molecular studies have identified the structural mechanism of action of UCP2 and have detailed the ways in which its expression and activity can be controlled at the transcriptional, translational and posttranslational levels. These studies suggest a number of ways in control of UCP2 expression and activity can be used therapeutically for both acute and chronic conditions. The development of such therapeutic approaches will greatly increase the tools available to combat a broad range of serious retinal diseases.

Authors+Show Affiliations

Department of Biochemistry, The University of Washington, Seattle, WA, 98109, USA.Department of Neural and Behavioral Sciences, The Pennsylvania State University, Hershey, PA, 17033, USA. Electronic address: cbarnstable@pennstatehealth.psu.edu.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

33422637

Citation

Hass, Daniel T., and Colin J. Barnstable. "Uncoupling Proteins in the Mitochondrial Defense Against Oxidative Stress." Progress in Retinal and Eye Research, vol. 83, 2021, p. 100941.
Hass DT, Barnstable CJ. Uncoupling proteins in the mitochondrial defense against oxidative stress. Prog Retin Eye Res. 2021;83:100941.
Hass, D. T., & Barnstable, C. J. (2021). Uncoupling proteins in the mitochondrial defense against oxidative stress. Progress in Retinal and Eye Research, 83, 100941. https://doi.org/10.1016/j.preteyeres.2021.100941
Hass DT, Barnstable CJ. Uncoupling Proteins in the Mitochondrial Defense Against Oxidative Stress. Prog Retin Eye Res. 2021;83:100941. PubMed PMID: 33422637.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Uncoupling proteins in the mitochondrial defense against oxidative stress. AU - Hass,Daniel T, AU - Barnstable,Colin J, Y1 - 2021/01/08/ PY - 2020/09/21/received PY - 2020/12/28/revised PY - 2021/01/03/accepted PY - 2022/07/01/pmc-release PY - 2021/1/11/pubmed PY - 2021/1/11/medline PY - 2021/1/10/entrez KW - Mitochondria KW - Neuroprotection KW - Reactive oxygen species (ROS) KW - Retina KW - UCP KW - Uncoupling SP - 100941 EP - 100941 JF - Progress in retinal and eye research JO - Prog Retin Eye Res VL - 83 N2 - Oxidative stress is a major component of most major retinal diseases. Many extrinsic anti-oxidative strategies have been insufficient at counteracting one of the predominant intrinsic sources of reactive oxygen species (ROS), mitochondria. The proton gradient across the inner mitochondrial membrane is a key driving force for mitochondrial ROS production, and this gradient can be modulated by members of the mitochondrial uncoupling protein (UCP) family. Of the UCPs, UCP2 shows a widespread distribution and has been shown to uncouple oxidative phosphorylation, with concomitant decreases in ROS production. Genetic studies using transgenic and knockout mice have documented the ability of increased UCP2 activity to provide neuroprotection in models of a number of diseases, including retinal diseases, indicating that it is a strong candidate for a therapeutic target. Molecular studies have identified the structural mechanism of action of UCP2 and have detailed the ways in which its expression and activity can be controlled at the transcriptional, translational and posttranslational levels. These studies suggest a number of ways in control of UCP2 expression and activity can be used therapeutically for both acute and chronic conditions. The development of such therapeutic approaches will greatly increase the tools available to combat a broad range of serious retinal diseases. SN - 1873-1635 UR - https://www.unboundmedicine.com/medline/citation/33422637/Uncoupling_proteins_in_the_mitochondrial_defense_against_oxidative_stress. L2 - https://linkinghub.elsevier.com/retrieve/pii/S1350-9462(21)00002-1 DB - PRIME DP - Unbound Medicine ER -
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