ArticleCell death discovery2024
Deptor protects against myocardial ischemia-reperfusion injury by regulating the mTOR signaling and autophagy.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
9 citing papers in PubMed.
- An oral-gut microbial metabolite linksGut microbes · 2026Article
- PARKIN overexpression confers cardioprotection via suppressing the mtDNA-cGAS-STING axis in myocardial ischemia/reperfusion injury.Basic research in cardiology · 2026Article
- Targeting the Gut-Brain-Ferroptosis Axis: Molecular Mechanisms and Therapeutic Potential in Alzheimer's Disease and Epilepsy.Journal of molecular neuroscience : MN · 2026Review
- Cardiomyocyte programmed cell death in dilated cardiomyopathy: molecular crosstalk and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- Propofol in combination with salvianolic acid A protect against lipopolysaccharide-induced cardiac dysfunction and ferroptosis through activating the SIRT1/FoxO1 signaling under diabetic condition.Annals of medicine · 2025Article
- Dysregulated Redox Signaling and Its Impact on Inflammatory Pathways, Mitochondrial Dysfunction, Autophagy and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Roles of Autophagy and Oxidative Stress in Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2025Review
- GSDME in cardiovascular diseases: research system and contemporary progress.Frontiers in immunology · 2025Review
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Deptor knockout mice were constructed by crossing Deptor Floxp3 mice with myh6 Cre mice, establishing a myocardial ischemia-reperfusion (I/R) model. Deptor knockout mice exhibited significantly increased myocardial infarction size and increased myocardial apoptosis in vivo. ELISA analysis indicated that the expression of CK-MB, LDH, and CtnT/I was significantly higher in the Deptor knockout mice. Deptor siRNA significantly reduced cell activity and increased myocardial apoptosis after I/R-induced in vitro. Deptor siRNA also significantly up-regulated the expression of p-mTOR, p-4EBP1, and p62, and down-regulated the expression of LC3 after I/R induction. Immunofluorescence indicated that LC3 dual fluorescence was weakened by Deptor knockout, and was enhanced after transfection with Deptor-overexpression plasmids. Treatment with OSI027, a co-inhibitor of mTORC1 and mTORC2, in either Deptor knockout mice or Deptor knockout H9C2 cells, resulted in a significant reduction in infarction size and apoptotic cardiomyocytes. ELISA analysis also showed that the expression of CK-MB, LDH, and CtnT/I were significantly down-regulated by treatment with OSI027. CCK-8 cell viability indicated that cell viability was enhanced, and the number of apoptotic cells was decreased in vitro following treatment with OSI027. These results revealed that OSI027 exerts a protective effect on myocardial ischemia/reperfusion injury in both an in vivo and in an in vitro model of I/R. These findings demonstrate that Deptor protects against I/R-induced myocardial injury by inhibiting the mTOR pathway and by increasing autophagy.
Identifiers
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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.