New Insights in Cardiac Ischemic Diseases

Dear Colleagues, 

Cardiac ischemic diseases are the most common causes of death worldwide. Ischemia-Reperfusion (I/R) process leads to O₂, metabolic and redox homeostasis alterations inducing tissue critical damages and/or contributing to the remodeling process as well as cardiac function alteration. Indeed, I/R triggers acute or chronic deleterious processes such as oxidative stress, inflammation, sympathetic nervous system activation, endoplasmic reticulum stress, mitochondrial function and dynamic alteration. In recent decades, we have advanced in our understanding of the biological and molecular pathways at the crosstalk of O₂ and metabolic homeostasis. More especially, the role of transcriptional activity (i.e., Hypoxia Inducible Factor-1, Nuclear factor-erythroid Factor 2-Related factor 2…) and post-translational modifications (i.e., phosphorylation, acetylation, citrullination, O-GlcNAcylation, Prolyl hydroxylation…) seems to represent innovative targets influencing I/R effects. Nevertheless, pre-clinical or clinical approaches addressing these issues are missing to improve our knowledge to explain deleterious consequences of I/R.

Thus, this Special Issue is dedicated to highlighting new pathways that contribute to the development of cardiac ischemic diseases. We aim to be able to bring a better knowledge for long-term efficient management of the disease. We invite investigators to present recent advances in the comprehension of the molecular pathways leading to acute and chronic response to I/R as well as the development of new approaches to prevent adverse consequences of I/R.

Dr. Delphine Baetz
Dr. Elise Belaïdi
Guest Editors

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