Epigenetics is defined as heritable changes in the pattern of post-translation modifications, which lead to the occurrence of new phenotypes without altering DNA sequences. Epigenetic modifications, mainly including DNA methylation, histone modifications, and chromatin remodeling, modulate gene transcription and expression. The processes are deposited by “writer” enzymes (adding the epigenetic marks), “reader” effector proteins (recognizing these marks) and “eraser” enzymes (removing these marks). Oxidative stress reflects the imbalance between the production of reactive oxygen species (ROS) and the scavenging capacity of an antioxidant system.

Excessive ROS, generated from various endogenous oxidative biochemical enzymes, interferes with the normal function of cells. Increasing evidence from preclinical and clinical studies has linked ROS to pathophysiology associated with aging-related diseases such as cardiovascular and fibrotic diseases. More recently, epigenetic modifications have been reported to participate in the control of stress stimuli and the mechanisms of aging, physiology and physiopathology, therefore affecting the occurrence and development of these diseases. Recently, it has been reported that asymmetrical arginine dimethylation of histone H4 by the protein arginine methylation transferase (PRMT1) is essential for oxidative stress-induced transcription activation, highlighting the epigenetic regulation of oxidative stress particularly in cardiovascular diseases. However, the related studies are still few, and the role of epigenetics in oxidative stress remains to be clarified.

This Special Issue aims to encourage researchers to submit original research and review articles focused on the discovery of novel epigenetic targets and drugs regulating oxidative stress in aging-related diseases, including but not limited to neurodegenerative diseases, cardiovascular diseases, fibrotic diseases, and cancer. We hope that the research of this Special Issue will improve our understanding of current and potential therapeutic strategies. We also hope that this provides an understanding of novel candidate drugs for treatment.

Potential topics include but are not limited to the following:

• Molecular mechanisms of epigenetic modifications (e.g., DNA methylation and histone methylation, acetylation, and succinylation) regulating oxidative stress
• Identification of novel epigenetic targets and signalling pathways participating in oxidative stress in aging-related diseases
• Drug discovery and rational design targeting epigenetic modifications via redox balance for the treatment of these diseases
• In vivo and in vitro studies focused on the epigenetics mechanism of small molecular drugs (i.e., natural and synthetic) regulating oxidative stress
• The role of oxidative stress in epigenetic cancer therapy, including anticancer drug-induced cardiotoxicity (e.g., for cardiac dysfunction, myocardial ischemia, thromboembolism, arterial and pulmonary hypertension)
• The role of epigenetic modifications in oxidative stress-induced cellular senescence
• The role of oxidative stress-induced epigenetic alterations in neurodegenerative diseases
• Discovery of novel epigenetic modification types modulating oxidative stress