Dear Colleagues,

Heart failure is the ultimate outcome of cardiovascular illness, caused by prolonged pressure overload (hypertension, myocardial ischemia or infarction), excessive volume load (mitral regurgitation), or genetic and acquired cardiomyopathies. Pathological molecular pathways in heart failure contribute to the alteration of cardiac structure, resulting in cardiac dysfunction. Within the intricate signaling network that defines myocardial remodeling, several distinct processes occur, including myocyte loss, cardiac hypertrophy, and changes in extracellular matrix homeostasis, fibrosis, impaired autophagy, metabolic abnormalities, and mitochondrial dysfunction. The complex physiological signaling networks that respond to the dual challenges of inflammatory and oxidative stress are major factors that promote the development of cardiovascular pathologies. Inhibition and/or attenuation of these signaling networks also delay the onset of cardiovascular diseases. Hence, acquiring a novel and in-depth comprehension of the atypical physiological processes and molecular mechanisms underlying heart failure is crucial to develop pioneering therapeutic approaches. 

In this research topic, we invite Original Research or Review articles that explore the molecular mechanisms behind heart failure and highlight the interplay between various signaling systems, along with potential treatments for cardiovascular medicine. In addition, we emphasize the influence of current therapys, such as natural substances or preexisting medications, on these molecular pathways and their potential for the advancement of heart failure therapy.

Dr. Ramoji Kosuru
Research Scientist-I
Guest Editor