ArticleThe Journal of clinical investigation2020
Upregulation of Rubicon promotes autosis during myocardial ischemia/reperfusion injury.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
What it found
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Who cites it
101 citing papers in PubMed, 144 citations in OpenAlex.
- Vps16 Attenuates Myocardial Ischemia/reperfusion Injury by Interacting with UVRAG and Activating Rab7.Cardiovascular drugs and therapy · 2026Article
- Mitophagy Facilitates Cytosolic Proteostasis to Preserve Cardiac Function.Circulation research · 2026Article
- Perm1 enhances Nrf2-driven antioxidant defense through Keap1 oxidation during myocardial ischemia/reperfusion injury.JCI insight · 2026Article
- Review
- Article
- Platelet Rubicon Bidirectional Regulation of GPVI and Integrin αIIbβ3 Signaling Mitigates Stroke Infarction Without Compromising Hemostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Osimertinib activates TFEB to trigger hepatocyte cytoplasmic vacuolation-associated cell death.Cell communication and signaling : CCS · 2026Article
- Review
- Mitochondrial programmed cell death in bronchopulmonary dysplasia: mechanisms and therapeutic targets.Frontiers in physiology · 2026Review
- Lysosomal homeostasis regulates myocardial ischemia-reperfusion injury through autophagy pathway.Scientific reports · 2025Article
- 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
- Mitochondrial quality control in cardiomyocytes: safeguarding the heart against disease and ageing.Nature reviews. Cardiology · 2025Review
- Acute Myocardial Infarction: Molecular Pathogenesis, Diagnosis, and Clinical Management.MedComm · 2025Review
- Regulated Cell Death in Myocardial Infarction.Circulation research · 2025Article
- Oxidative Stress in the Regulation of Autosis-Related Proteins.Antioxidants (Basel, Switzerland) · 2025Review
- Thapsigargin triggers a non-apoptotic, caspase-independent programmed cell death in basophilic leukaemia cells.Cell death discovery · 2025Article
- Organellophagy regulates cell death:A potential therapeutic target for inflammatory diseases.Journal of advanced research · 2025Review
- The link between ferroptosis and autophagy in myocardial ischemia/reperfusion injury: new directions for therapy.Journal of cardiovascular translational research · 2025Review
- The inducible role of autophagy in cell death: emerging evidence and future perspectives.Cell communication and signaling : CCS · 2025Review
41 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Although autophagy is generally protective, uncontrolled or excessive activation of autophagy can be detrimental. However, it is often difficult to distinguish death by autophagy from death with autophagy, and whether autophagy contributes to death in cardiomyocytes (CMs) is still controversial. Excessive activation of autophagy induces a morphologically and biochemically defined form of cell death termed autosis. Whether autosis is involved in tissue injury induced under pathologically relevant conditions is poorly understood. In the present study, myocardial ischemia/reperfusion (I/R) induced autosis in CMs, as evidenced by cell death with numerous vacuoles and perinuclear spaces, and depleted intracellular membranes. Autosis was observed frequently after 6 hours of reperfusion, accompanied by upregulation of Rubicon, attenuation of autophagic flux, and marked accumulation of autophagosomes. Genetic downregulation of Rubicon inhibited autosis and reduced I/R injury, whereas stimulation of autosis during the late phase of I/R with Tat-Beclin 1 exacerbated injury. Suppression of autosis by ouabain, a cardiac glycoside, in humanized Na+,K+-ATPase-knockin mice reduced I/R injury. Taken together, these results demonstrate that autosis is significantly involved in I/R injury in the heart and triggered by dysregulated accumulation of autophagosomes due to upregulation of Rubicon.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.