From Defence to Dysfunction: The Dual Role of Autophagy and Mitophagy in Cardiomyopathy

Cardiomyopathy is a disease unique to the heart muscle that increases a patient's risk of death due to heart failure, contrary to vascular conditions. Cellular powerhouses called mitochondria produce oxygen species that are reactive, that may damage both the mitochondria as well as the heart muscle if they are not managed. They also provide energy for contractions in the heart. Maintaining proper heart function both at base and in reaction to various stress and illness circumstances depends on autophagy as well as mitochondrial autophagy, which eliminates damaged mitochondria. Understanding the pathogenesis of heart diseases, which includes a wide spectrum of cardiovascular problems connected to related cardiomyopathies, is still hampered by autophagy and mitophagy. Additionally, heart failure continues to be a primary source of increased morbidity among people with cardiomyopathy, despite notable advances in lowering death rates from cardiovascular diseases (CVDs). Due to their role in the development of cardiovascular conditions, these cellular processes are appealing targets for diagnosis and therapy. They are crucial for preserving cellular equilibrium and eliminating damaged or malfunctioning components. Further, cardiomyopathies remain a major concern despite the availability of several traditional diagnostic and treatment approaches. Thus, we are going to explore the possible autophagy and mitophagy in the development and progression of cardiomyopathy and provide an overview of current research in this area in this review.