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Find out about the importance of autophagy in heart disease with our free pathway. This pathway highlights the triggers of autophagy, such as hypoxia or nutrient starvation, and how autophagy helps maintain cell homeostasis.
Download our autophagy in heart disease pathway
Autophagy is an evolutionarily conserved, lysosomal pathway of engulfment, degradation, and recycling of cellular contents, including long-lived proteins and organelles. Autophagy gets its name from the Greek words for self (auto) and to eat (phagein). Autophagy promotes cell survival, maintaining cellular homeostasis under resting and stress conditions. It is a tightly regulated response that can allow cells to remove unwanted proteins and organelles.
Numerous stimuli can induce autophagy – for example, hypoxia and nutrient starvation – which enable the cell to free vital amino acids to re-use as well as clear aberrant structures or organelles. Autophagy involves a series of sequential steps that start with initiation/sequestration, continue with fusion with lysosomes, ultimately leading to degradation.
Initiation of autophagy occurs when a double membrane forms within the cytoplasm that non-selectively engulfs proteins and structures. Autophagy-mediated degradation of specific proteins and organelles can occur via targeting proteins.
Autophagy plays a critical role in multiple clinical disorders, including heart disease. Studies have shown that both autophagy and mitophagy are important for the preservation of cardiovascular homeostasis. After experiencing a myocardial infarction, cardiomyocytes will undergo remodeling and dysfunction through the activation of autophagy, which can lead to heart failure. Therefore, studying the mechanisms of autophagy activation is a key area of research in the prevention of heart disease.
To view all key proteins involved in the autophagy process in heart disease, download our pathway.