Role of Oxidative Stress in Cardiac Remodeling and Heart Failure

Dear Colleagues,

Cardiac remodeling is defined as molecular, cellular, and interstitial cardiac changes that manifest clinically as changes in the size, shape, and function of the heart. Cardiac failure is the final pathway of many cardiac diseases and presents a major public health issue due to its poor prognosis and high prevalence, morbidity, and mortality. Oxidative stress is characterized by an increased ratio between oxygen radical production and scavenging capacity. Although at low levels reactive oxygen species play a role in intracellular signaling pathways, at higher levels they may induce cellular injury, dysfunction, and death. Clinical and experimental studies have shown that oxidative stress is increased in the myocardium and at a systemic level during heart failure, and in the myocardium, increased oxidative stress may result from injured myocytes and may induce additional lesions to myocardial cells, therefore forming a vicious cycle. Despite extensive studies, the molecular pathways involved in heart failure-associated oxidative stress are still not completely understood.

This Special Issue is dedicated to reviews and original research regarding in vitro, animal experiments, and clinical studies about the mechanisms underlying the role of increased oxidative stress in cardiac remodeling and heart failure pathophysiology, clinical manifestations, novel targets, and pharmacological and non-pharmacological treatment.

Dr. Marina Politi Okoshi
Guest Editor

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