Interacting with thioredoxin-1-disease or no disease?

Tim Christian Zschauer, Shoji Matsushima, Joachim Altschmied, Dan Shao, Junichi Sadoshima, Judith Haendeler

Research output: Contribution to journalReview article

24 Citations (Scopus)

Abstract

Significance: Many cardiovascular disorders are accompanied by a deregulated cellular redox balance resulting in elevated levels of intracellular reactive oxygen species (ROS). One major antioxidative cellular molecule is thioredoxin-1 (Trx-1). Its indispensability is demonstrated by the embryonic lethality of Trx-1 deficient mice. Trx-1 is ubiquitously expressed in cells and has numerous, diverse functions. It not only reduces oxidized proteins or, together with peroxiredoxins, detoxifies H2O2, but also binds to several proteins and thereby regulates their functions. The interaction partners of Trx-1 differ depending on its localization in the cytosol or in the nucleus. Recent Advances/Critical Issues: Over the past decade it has become clear that Trx-1 is not only critical for tumor functions, which has resulted in therapeutic approaches targeting this protein, but also essential for proper functions of the vasculature and the heart. Changes in post-translational modifications of Trx-1 or in its interactions with other proteins can lead to a switch from a physiologic state of cells and organs to diverse pathologies. This review provides insights into the role of Trx-1 in different physiological situations and cardiac hypertrophy, ischemia reperfusion injury, heart failure, atherosclerosis, and diabetes mellitus type 2, underscoring the central role of Trx-1 in cardiovascular health and disease. Future Directions: Thus, the manipulation of Trx-1 activity in the heart and/or vasculature, for example, by small molecules, seems to be a promising therapeutic option in cardiovascular diseases, as general anti-oxidant treatments would not take into account interactions of Trx-1 with other proteins and also eliminate vital ROS.

Original languageEnglish
Pages (from-to)1053-1062
Number of pages10
JournalAntioxidants and Redox Signaling
Volume18
Issue number9
DOIs
Publication statusPublished - Mar 20 2013
Externally publishedYes

Fingerprint

Thioredoxins
Proteins
Reactive Oxygen Species
Cardiovascular Diseases
Peroxiredoxins
Molecules
Cardiomegaly
Pathology
Protein Transport
Post Translational Protein Processing
Medical problems
Reperfusion Injury
Oxidants
Cytosol
Type 2 Diabetes Mellitus
Oxidation-Reduction
Tumors
Atherosclerosis
Heart Failure
Switches

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

Cite this

Zschauer, T. C., Matsushima, S., Altschmied, J., Shao, D., Sadoshima, J., & Haendeler, J. (2013). Interacting with thioredoxin-1-disease or no disease? Antioxidants and Redox Signaling, 18(9), 1053-1062. https://doi.org/10.1089/ars.2012.4822

Interacting with thioredoxin-1-disease or no disease? / Zschauer, Tim Christian; Matsushima, Shoji; Altschmied, Joachim; Shao, Dan; Sadoshima, Junichi; Haendeler, Judith.

In: Antioxidants and Redox Signaling, Vol. 18, No. 9, 20.03.2013, p. 1053-1062.

Research output: Contribution to journalReview article

Zschauer, TC, Matsushima, S, Altschmied, J, Shao, D, Sadoshima, J & Haendeler, J 2013, 'Interacting with thioredoxin-1-disease or no disease?', Antioxidants and Redox Signaling, vol. 18, no. 9, pp. 1053-1062. https://doi.org/10.1089/ars.2012.4822
Zschauer TC, Matsushima S, Altschmied J, Shao D, Sadoshima J, Haendeler J. Interacting with thioredoxin-1-disease or no disease? Antioxidants and Redox Signaling. 2013 Mar 20;18(9):1053-1062. https://doi.org/10.1089/ars.2012.4822
Zschauer, Tim Christian ; Matsushima, Shoji ; Altschmied, Joachim ; Shao, Dan ; Sadoshima, Junichi ; Haendeler, Judith. / Interacting with thioredoxin-1-disease or no disease?. In: Antioxidants and Redox Signaling. 2013 ; Vol. 18, No. 9. pp. 1053-1062.
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