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. 2023 Apr 3:11:1164681.
doi: 10.3389/fcell.2023.1164681. eCollection 2023.

Autosis as a selective type of cell death

Lingge Bai  1 , Qiong Wu  1 , Xinyue Zhang  1 , Yuting Zhao  1
Affiliations

Autosis as a selective type of cell death

Lingge Bai et al. Front Cell Dev Biol. .

Erratum in

No abstract available

Keywords: Beclin 1; Na+/K+-ATPase; Tat-BECN1 peptide; autophagic cell death; autophagy; autosis; cardiac glycosides.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
(A) Selectivity of autosis. During renal ischemia/reperfusion, pericytes undergo autosis (with morphological features such as focal swelling of the perinuclear space), but not tubular cells or endothelial cells. Upon treatment with Tat-BECN1 peptide or other autosis inducers, HIV-1-infected cells (macrophages or CD4+ T cells) undergo autosis, but not uninfected cells. Upon treatment with Tat-BECN1 peptide or other autosis inducers, or oncolytic virus-infected CAR-T cells, tumor cells undergo autosis, but not non-tumor cells. (B) Regulation of autosis. Class III PI3K complexes and Na+/K+-ATPase are two major mediators of autosis, which interact through Beclin 1 and alpha subunits. Pharmacologically, the interaction is enhanced by autosis inducer Tat-BECN1 peptide and blocked by autosis inhibitor cardiac glycosides. Regulatory proteins of autosis act on Class III PI3K complexes by 1) transcriptional regulation, 2) post-translational modifications, and 3) protein–protein interactions. Autosis occurs in vivo, in the brain during cerebral hypoxia/ischemia, in the kidney during renal ischemia/reperfusion, in the heart during cardiac ischemia/reperfusion, in the liver during anorexia nervosa, and in the skin during terminal differentiation of keratinocyte lineage cells.
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