ArticleThe Journal of biological chemistry2019
Tumor susceptibility gene 101 ameliorates endotoxin-induced cardiac dysfunction by enhancing Parkin-mediated mitophagy.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Two Routes for Removing Unhealthy Mitochondria: Degradation and Secretion.Circulation research · 2026Review
- Mitochondria-Derived Vesicles and Mitochondrial Extracellular Vesicles in Health and Cardiovascular Disease.Circulation research · 2026Review
- c-FLIP Protects Cardiac Microcirculation in Sepsis-Induced Myocardial Dysfunction Via FUNDC1-Mediated Regulation of Mitochondrial Autophagy.JACC. Basic to translational science · 2025Article
- Tsg101 mimicry of canonical E2 enzymes underlies its role in ubiquitin signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Nitric oxide-primed engineered extracellular vesicles restore bioenergetics in acute kidney injury via mitochondrial transfer.Theranostics · 2025Article
- Autophagy-Dependent Secretion: Crosstalk between Autophagy and Exosome Biogenesis.Current issues in molecular biology · 2024Review
- Research Progress on Mechanisms and Treatment of Sepsis-Induced Myocardial Dysfunction.International journal of general medicine · 2024Review
- Changes in the components of salivary exosomes due to initial periodontal therapy.Journal of periodontal & implant science · 2023Article
- Mitochondria-endoplasmic reticulum contacts in sepsis-induced myocardial dysfunction.Frontiers in cell and developmental biology · 2022Review
- Article
- LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis.Inflammation · 2021Article
- Mechanism of Mitophagy and Its Role in Sepsis Induced Organ Dysfunction: A Review.Frontiers in cell and developmental biology · 2021Review
- Aldehyde Dehydrogenase 2 Protects Against Lipopolysaccharide-Induced Myocardial Injury by Suppressing Mitophagy.Frontiers in pharmacology · 2021Article
- Comprehensive Mechanism, Novel Markers and Multidisciplinary Treatment of Severe Acute Pancreatitis-Associated Cardiac Injury - A Narrative Review.Journal of inflammation research · 2021Review
- Targeting PINK1 Using Natural Products for the Treatment of Human Diseases.BioMed research international · 2021Review
- Article
- Tsg101 positively regulates P62-Keap1-Nrf2 pathway to protect hearts against oxidative damage.Redox biology · 2020Article
- The Multifaceted Roles of the Tumor Susceptibility Gene 101 (TSG101) in Normal Development and Disease.Cancers · 2020Review
- Mitochondrial Quality Control and Cellular Proteostasis: Two Sides of the Same Coin.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Cardiac mitochondrial damage and subsequent inflammation are hallmarks of endotoxin-induced myocardial depression. Activation of the Parkin/PTEN-induced kinase 1 (PINK1) pathway has been shown to promote autophagy of damaged mitochondria (mitophagy) and to protect from endotoxin-induced cardiac dysfunction. Tumor susceptibility gene 101 (TSG101) is a key member of the endosomal recycling complexes required for transport, which may affect autophagic flux. In this study, we investigated whether TSG101 regulates mitophagy and influences the outcomes of endotoxin-induced myocardial dysfunction. TSG101 transgenic and knockdown mice underwent endotoxin/lipopolysaccharide treatment (10 μg/g) and were assessed for survival, cardiac function, systemic/local inflammation, and activity of mitophagy mediators in the heart. Upon endotoxin challenge and compared with WT mice, TSG101 transgenic mice exhibited increased survival, preserved cardiac contractile function, reduced inflammation, and enhanced mitophagy activation in the heart. By contrast, TSG101 knockdown mice displayed opposite phenotypes during endotoxemia. Mechanistically, both coimmunoprecipitation assays and coimmunofluorescence staining revealed that TSG101 directly binds to Parkin in the cytosol of myocytes and facilitates translocation of Parkin from the cytosol to the mitochondria. Our results indicate that TSG101 elevation could protect against endotoxin-triggered myocardial injury by promoting Parkin-induced mitophagy.
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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.