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Thioredoxin in the cardiovascular system

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Abstract

The thioredoxin (TRX) system (TRX, TRX reductase, and NADPH) is a ubiquitous thiol oxidoreductase system that regulates cellular reduction/oxidation (redox) status. The impairment of cell redox state alters multiple cell pathways, which may contribute to the pathogenesis of cardiovascular disorders including hypertension, atherosclerosis, and heart failure. In this manuscript, we review the essential roles that TRX plays by limiting oxidative stress directly via antioxidant effects and indirectly by protein–protein interactions with key signaling molecules such as thioredoxin interacting protein (TXNIP). TRX and its endogenous regulators may represent important future targets to develop clinical therapies for diseases associated with oxidative stress.

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Abbreviations

ASK1:

Apoptosis signal-regulating kinase 1

EC:

Endothelial cell

JNK:

Jun N-terminal kinase

PDGF:

Platelet-derived growth factor

ROS:

Reactive oxygen species

TRX:

Thioredoxin

TXNIP:

TRX-interacting protein

VCAM:

Vascular cell adhesion molecule

VSMC:

Vascular smooth muscle cell

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Acknowledgment

This study was supported by the NIH grants (HL-62826 and HL-64839) to BCB.

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Correspondence to Bradford C. Berk.

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World, C.J., Yamawaki, H. & Berk, B.C. Thioredoxin in the cardiovascular system. J Mol Med 84, 997–1003 (2006). https://doi.org/10.1007/s00109-006-0109-6

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