Cellular Stress Response and Cardiovascular Aging Related Diseases

Responses to stress, arising from physiological processes and/or external stimuli, is an integral part of cardiovascular physiology and pathology. To deal with stress, cells, including cardiomyocytes, have evolved various mechanisms, such as heat shock response, DNA damage response, unfolded protein response, oxidative stress response, and so on. Such mechanisms of cellular adaptation to ensure the survival of stress-adapted cells in challenging conditions and the negative selection of damaged cells. Nevertheless, prolonged or severe stress that cannot be managed by adaptive mechanisms generally culminate with the cellular senescence or elimination of stressed cells, and hence result in cardiovascular aging and related disorders. Thus, the identities of the cellular stress corrective strategies are important targets for the development of therapeutic approaches for cardiovascular aging related diseases.

The purpose of this research topic is to explore the relationship between cellular stress response and cardiovascular aging related diseases (such as arteriosclerosis, myocardial infarction, vascular calcification, heart failure, etc.) and the potential interferences by identifying the cellular stress corrective strategies to relieve cardiovascular aging.

The subtopics include but are not limited to the following:
• The potential role of heat shock response on cardiovascular aging related diseases;
• The effects of persistent genomic and/or mitochondrial DNA damage on cardiovascular aging related diseases;
• Underlying mechanisms of inducing unfolded protein responses (UPR) on endoplasmic reticulum (UPRER) or mitochondrial (UPRmt) during the occurrence and development of cardiovascular aging related diseases;
• The mechanism of stress caused by heme deprivation on cardiovascular aging related diseases, and the interventions to reverse the stress response;
• The possible mechanism that promotes integrated stress response on the progression of cardiovascular aging related diseases;
• Rebuilding the barrier of reactive oxygen species (ROS), and investigating other feasible strategies to correct the oxidative stress response in the improvement of cardiovascular aging related diseases.