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Autosis: A New Target to Prevent Cell Death
Jihoon Nah1, Daniela Zablocki1, Junichi Sadoshima1
1Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, Newark, New Jersey.
JACC. Basic to Translational Science
|September 3, 2020
Summary
Excessive autophagy causes autosis, a cell death linked to heart injury during reperfusion. Understanding autosis mechanisms may reveal new ways to protect the heart from stress.
Area of Science:
- Cardiology
- Cell Biology
- Pathology
Background:
- Autophagy is a cellular process with dual roles in cell survival and death.
- Excessive autophagy can lead to a specific form of programmed cell death known as autosis.
- Autosis is implicated in cellular damage during pathological conditions like ischemia-reperfusion.
Purpose of the Study:
- To review the unique characteristics of autosis.
- To discuss the role of autosis in myocardial injury.
- To explore the molecular mechanisms underlying autosis.
Main Methods:
- Literature review of studies on autophagy and cell death.
- Analysis of morphological and biochemical features of autosis.
- Examination of autosis's involvement in myocardial ischemia-reperfusion injury.
Main Results:
- Autosis is characterized by perinuclear space ballooning and cardiac glycoside sensitivity.
- Autosis occurs during the late phase of myocardial reperfusion and contributes to injury.
- The molecular pathways driving autosis are complex and require further elucidation.
Conclusions:
- Autosis is a distinct cell death pathway activated by excessive autophagy.
- Autosis plays a significant role in myocardial injury following ischemia-reperfusion.
- Targeting autosis pathways may offer novel therapeutic strategies for cardiac protection.
Keywords:
ATG, autophagy-relatedATPase, adenosine triphosphataseER, endoplasmic reticulumHIV, human immunodeficiency virusI/R, ischemia-reperfusionLBR, lamin B receptorNa+,K+–adenosine triphosphatasePI3K, phosphatidylinositol 3 kinasePNS, perinuclear spaceTat, transactivation of transcriptionautophagic cell deathautophagic fluxautosisbeclin 1rubicon
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