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Cited by 352

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Thiol-based mechanisms of the thioredoxin and glutaredoxin systems: implications for diseases in the cardiovascular system

Berndt, Carsten, Lillig, Christopher Horst, Holmgren, Arne·2007·American Journal of Physiology-Heart and Circulatory Physiology

Abstract

Reactive oxygen species (ROS) and the cellular thiol redox state are crucial mediators of multiple cell processes like growth, differentiation, and apoptosis. Excessive ROS production or oxidative stress is associated with several diseases, including cardiovascular disorders like ischemia-reperfusion. To prevent ROS-induced disorders, the heart is equipped with effective antioxidant systems. Key players in defense against oxidative stress are members of the thioredoxin-fold family of proteins. Of these, thioredoxins and glutaredoxins maintain a reduced intracellular redox state in mammalian cells by the reduction of protein thiols. The reversible oxidation of Cys-Gly-Pro-Cys or Cys-Pro(Ser)-Tyr-Cys active site cysteine residues is used in reversible electron transport. Thioredoxins and glutaredoxins belong to corresponding systems consisting of NADPH, thioredoxin reductase, and thioredoxin or NADPH, glutathione reductase, glutathione, and glutaredoxin, respectively. Thioredoxin as well as glutaredoxin activities appear to be very important for the progression and severity of several cardiovascular disorders. These proteins function not only as antioxidants, they inhibit or activate apoptotic signaling molecules like apoptosis signal-regulating kinase 1 and Ras or transcription factors like NF-κB. Thioredoxin activity is regulated by the endogenous inhibitor thioredoxin-binding protein 2 (TBP-2), indicating an important role of the balance between thioredoxin and TBP-2 levels in cardiovascular diseases. In this review, we will summarize cardioprotective effects of endogenous thioredoxin and glutaredoxin systems as well as the high potential in clinical applications of exogenously applied thioredoxin or glutaredoxin or the induction of endogenous thioredoxin and glutaredoxin systems.

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Crossref · 10.1152/ajpheart.01162.2006

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Metadata

Authors
Berndt, C., Lillig, C. H., & Holmgren, A.
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Published
2007-03
Volume
292
Issue
3
Pages
H1227-H1236
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
OpenAlex
W2113714326
Cited by
352
References
11
FWCI
8.47
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Thiol-based mechanisms of the thioredoxin and glutaredoxin systems: implications for diseases in the cardiovascular system. https://app.cochat.ai/papers/10.1152/ajpheart.01162.2006
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Berndt, C., Lillig, C. H., & Holmgren, A. (2007). Thiol-based mechanisms of the thioredoxin and glutaredoxin systems: implications for diseases in the cardiovascular system. American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.01162.2006

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