ArticleCells2022
Tfeb-Mediated Transcriptional Regulation of Autophagy Induces Autosis during Ischemia/Reperfusion in the Heart.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Theaflavin attenuates atherosclerosis by targeting GSK-3β to suppress pyroptosis and Promote Autophagy in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Article
- The geroprotective potential of chalcones.Nature communications · 2025Review
- The protective effects of retinoic acid-induced protein 14 on ischemia/reperfusion-induced myocardial apoptosis involves over-autophagy repression.Experimental animals · 2025Article
- Acute Myocardial Infarction: Molecular Pathogenesis, Diagnosis, and Clinical Management.MedComm · 2025Review
- The inducible role of autophagy in cell death: emerging evidence and future perspectives.Cell communication and signaling : CCS · 2025Review
- Autosis: a new form of cell death in myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2025Review
- Mitochondria as the central regulator of cell death in bronchopulmonary dysplasia.Frontiers in physiology · 2025Review
- The multifaceted role of autophagy and mitophagy in cardiovascular health and disease.Autophagy reports · 2025Review
- Neuronal autosis is NaCell death & disease · 2024Article
- Deficiency of diacylglycerol Kinase ζ promotes Beclin1-mediated autophagyInternational journal of medical sciences · 2024Article
- Autophagy: Regulator of cell death.Cell death & disease · 2023Review
- NPPA/atrial natriuretic peptide is an extracellular modulator of autophagy in the heart.Autophagy · 2023Article
- Autosis as a selective type of cell death.Frontiers in cell and developmental biology · 2023Article
- Autophagy, innate immunity, and cardiac disease.Frontiers in cell and developmental biology · 2023Review
- Targeting the Autophagy-Lysosome Pathway in a Pathophysiologically Relevant Murine Model of Reversible Heart Failure.JACC. Basic to translational science · 2022Article
- Mechanisms of Ischemic Heart Injury.Cells · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
Autosis is a unique form of cell death with characteristic morphological and biochemical features caused by dysregulated autophagy. Autosis is observed in the heart during the late phase of ischemia/reperfusion (I/R), when marked accumulation of autophagosomes is induced. We previously showed that the excessive accumulation of autophagosomes promotes autosis in cardiomyocytes. Although the inhibition of autophagic flux via the upregulation of Rubicon induces the accumulation of autophagosomes during I/R, it appears that additional mechanisms exacerbating autophagosome accumulation are required for the induction of autosis. Here, we show that Tfeb contributes to the induction of autosis during the late phase of I/R in the heart. During myocardial reperfusion, Tfeb is activated and translocated into the nucleus, which in turn upregulates genes involved in autophagy and lysosomal function. The overexpression of Tfeb enhanced cardiomyocyte death induced by a high dose of TAT-Beclin 1, an effect that was inhibited by the downregulation of Atg7. Conversely, the knockdown of Tfeb attenuated high-dose TAT-Beclin1-induced death in cardiomyocytes. Although the downregulation of Tfeb in the heart significantly decreased the number of autophagic vacuoles and inhibited autosis during I/R, the activation of Tfeb activity via 3,4-dimethoxychalcone, an activator of Tfeb, aggravated myocardial injury during I/R. These findings suggest that Tfeb promotes cardiomyocyte autosis during the late phase of reperfusion in the heart.
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