期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 32, 期 10, 页码 677-700出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2019.7963
关键词
fatty liver disease; NAFLD; NASH; hindlimb ischemia; peripheral artery disease
资金
- National Institute of Health [R01 DK103750, R01 HL133013, R21 AG058983, R21 AA026922, R01 HL137771, R03 AG 051857]
- American Heart Association [16GRNT27660006]
- European Cooperation in Science and Technology (COST Action) [BM1203/EU-ROS]
- Metabolic Clinical Research Collaborative
- NIH/Boston University Clinical & Translational Science Institute [1UL1TR001430]
- Evans Junior Faculty Research Award by the Department of Medicine of Boston University
- NIH through the Whitaker Cardiovascular Institute at Boston University [T32 HL007224]
Critical Issues: Glutaredoxins mainly catalyze the removal of protein-bound GSH and help maintain protein thiols in a highly reduced state without exerting direct antioxidant properties. Conversely, glutathione S-transferase (GST), peroxiredoxins, and occasionally glutaredoxins can also catalyze protein S-glutathionylation, thus promoting a dynamic redox environment. Recent Advances: The latest studies of glutaredoxin-1 (Glrx) transgenic or knockout mice demonstrate important distinct roles of Glrx in a variety of pathologies. Endogenous Glrx is essential to maintain normal hepatic lipid homeostasis and prevent fatty liver disease. Further, in vivo deletion of Glrx protects lungs from inflammation and bacterial pneumonia-induced damage, attenuates angiotensin II-induced cardiovascular hypertrophy, and improves ischemic limb vascularization. Meanwhile, exogenous Glrx administration can reverse pathological lung fibrosis. Future Directions: Although S-glutathionylation modifies many proteins, these studies suggest that S-glutathionylation and Glrx regulate specific pathways in vivo, and they implicate Glrx as a potential novel therapeutic target to treat diverse disease conditions.
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