Excessive autophagy induces a defined form of cell death called autosis, which is characterized by unique morphological features, including ballooning of perinuclear space and biochemical features, including sensitivity to cardiac glycosides. Autosis is observed during the late phase of reperfusion after a period of ischemia and contributes to myocardial injury. This review discusses unique features of autosis, the involvement of autosis in myocardial injury, and the molecular mechanism of autosis. Because autosis promotes myocardial injury under some conditions, a better understanding of autosis may lead to development of novel interventions to protect the heart against myocardial stress.
Keywords: ATG, autophagy-related; ATPase, adenosine triphosphatase; ER, endoplasmic reticulum; HIV, human immunodeficiency virus; I/R, ischemia-reperfusion; LBR, lamin B receptor; Na+,K+–adenosine triphosphatase; PI3K, phosphatidylinositol 3 kinase; PNS, perinuclear space; Tat, transactivation of transcription; autophagic cell death; autophagic flux; autosis; beclin 1; rubicon.
© 2020 The Authors.