Abstract
In the issue of International Journal of Cardiology, Hemling P. et al. describe that the impairment of thioredoxin (TRX) activity is partially responsible for reactive oxygen species (ROS) accumulation in hyperglycaemic endothelial cells (EC). Interestingly, authors extend this finding to placental arterial EC where the employment of TRX synthetic peptides is able to restore physiological levels of ROS and subsequent improvement of the VEGF-A response, which is diminished in diabetic conditions [1]. The article sheds light on the biological impact of TRX-based as a link between the redox systems and endothelial function in hyperglycaemia.
| Original language | English |
|---|---|
| Pages (from-to) | 82-83 |
| Number of pages | 2 |
| Journal | International Journal of Cardiology |
| Volume | 308 |
| Early online date | 23 Mar 2020 |
| DOIs | |
| Publication status | Published - 1 Jun 2020 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
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