Transcriptional Mechanisms for Redox Stress in the Cardiovascular System
A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "RNA".
Deadline for manuscript submissions: closed (20 December 2022) | Viewed by 2489
Special Issue Editor
Interests: redox biology; cardiac biology; cardiac hypertrophy; heart failure; Nrf2 signaling; cardiac ageing; cardiomyopathy; proteotoxicity and proteostasis; arrhythmia; atrial remodeling
Special Issue Information
Dear Colleagues,
We have come a long way in understanding the role of redox processes in the cardiovascular system under basal and stress conditions. In particular, changes in the redox state toward either of the arms (i.e., oxidative or reductive) influences cardiac development, metabolism, physiology, and pathology, including atherosclerosis, cardiomyopathy, ischemic/reperfusion injury, and heart failure. The interplay between oxidants (ROS/RNS) and reductants (antioxidants) controls various physiological pathways and stress responses. However, the relationship has so far proven to be more complex and intricately regulated. For instance, the disappointing clinical expectations of antioxidant treatments are evidence of this nature as we begin to understand the balance between the two. In part, this might be due to the fact that while reductive or oxidative stress seems to be detrimental, a moderate pro-oxidative condition exerting a eustress is desired by myocytes for acting as electron donors for cellular signaling and function. It is imperative that we apply newer concepts and ideas to unravel this gap in knowledge. In this juncture, understanding the global changes in myocardial transcriptome and associated effects in the heart at basal and disease settings will facilitate the scientific community, pharmaceutical industry, healthcare professionals, as well as the public with up-to-date knowledge to improve cardiac health and outcomes.
This brings us to the message of this Special Issue that emphasizes discovering novel mechanisms in irremediable heart diseases involving excess/insufficient oxidants (i.e., ROS/RNS) or reductants (i.e., antioxidants) at the level of transcriptional regulation and gene expression. Our aim here is to better understand pathophysiology to design preventive and therapeutic strategies through enhanced knowledge on gene regulation/transcription. Therefore, we provide recent insights into the field of redox biology in the context of heart diseases, including cardiac hypertrophy, coronary artery disease, heart failure, arrhythmia, hypertension, and stroke. We hope this will inspire further lines of research.
Dr. Rajasekaran Namakkal-Soorappan
Guest Editor
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Keywords
- gene regulation
- Nrf2-antioxidant signaling
- transcription factors
- myocardial transcriptome
- redox transcriptome
- epigenetic regulation
- redox stress
