ArticleFASEB bioAdvances2020
Thrombospondin-1 mediates Drp-1 signaling following ischemia reperfusion in the aging heart.
Article in FASEB bioAdvances, 2020. 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, 22 citations in OpenAlex.
- ITCH-Mediated Ubiquitination and Degradation of THBS1: A Key Mechanism for Enhancing Mitochondrial Biogenesis and Alleviating Mouse Skeletal Muscle Atrophy.Acta physiologica (Oxford, England) · 2026Article
- p16EMBO reports · 2026Article
- Aging Mediates Inflammatory Transformation of Kidney-Resident Macrophages via Thrombospondin-1 Signaling.Immune network · 2025Article
- Establishing and Validating a Biomolecular Signature of Ischemia/Reperfusion Injury in a Porcine Pancreas Allotransplantation Model.Transplantation direct · 2025Article
- Mitochondrial transplantation combined with coenzyme QExperimental physiology · 2025Article
- Molecular Mechanisms and Potential Therapeutic Targets of Ischemia-Reperfusion Injury in Kidney Transplantation.Current issues in molecular biology · 2025Review
- Differential regulation by CD47 and thrombospondin-1 of extramedullary erythropoiesis in mouse spleen.eLife · 2024Article
- Differential regulation by CD47 and thrombospondin-1 of extramedullary erythropoiesis in mouse spleen.bioRxiv : the preprint server for biology · 2024Article
- Association of mitochondrial homeostasis and dynamic balance with malignant biological behaviors of gastrointestinal cancer.Journal of translational medicine · 2023Review
- Adipose stromal vascular fraction reverses mitochondrial dysfunction and hyperfission in aging-induced coronary microvascular disease.American journal of physiology. Heart and circulatory physiology · 2022Article
- Downregulation of SIRT3 Aggravates Lung Ischemia Reperfusion Injury by Increasing Mitochondrial Fission and Oxidative Stress through HIF-1Oxidative medicine and cellular longevity · 2022Article
- Current Understanding of the Pivotal Role of Mitochondrial Dynamics in Cardiovascular Diseases and Senescence.Frontiers in cardiovascular medicine · 2022Review
- Thrombospondin 1 in Metabolic Diseases.Frontiers in endocrinology · 2021Review
- Potential Therapies to Protect the Aging Heart Against Ischemia/Reperfusion Injury.Frontiers in cardiovascular medicine · 2021Review
- Coronary microvascular injury in myocardial infarction: perception and knowledge for mitochondrial quality control.Theranostics · 2021Review
- SIRT1/SIRT3 Modulates Redox Homeostasis during Ischemia/Reperfusion in the Aging Heart.Antioxidants (Basel, Switzerland) · 2020Review
- Thrombospondin-1 mediates Drp-1 signaling following ischemia reperfusion in the aging heart.FASEB bioAdvances · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIschemia reperfusion (IR) injury leads to activation of dynamin-related protein (Drp-1), causing mitochondrial fission and generation of reactive oxygen species (ROS), but the molecular mechanisms that activate Drp-1 are not known. The purpose of this study was to establish a link between Thbs-1 and fission protein (Drp-1) through Pgc-1α following IR in advancing age.
methodsFemale Fischer-344 rats were divided into four groups: Young Control, Young + IR, Old Control, and Old + IR. Heart function and coronary flow were evaluated at baseline and 72 hours after IR, hearts were explanted and mitochondrial ROS generation was measured using MitoPY1, as well as protein levels of Thbs-1, Pgc-1α, and Drp-1. In vitro, rat aortic endothelial cells (RAEC) were treated with siRNA or plasmid for Pgc-1α to evaluate Pgc-1α effect on Drp-1.
resultsMitochondrial ROS generation in heart tissue increased in both age groups following IR. Old animals exhibited diastolic dysfunction at baseline; after IR they displayed reduced systolic function and exacerbated diastolic dysfunction compared to young controls. IR increased Thbs-1 and Drp-1 expression in young and old hearts compared to control. siRNA to Pgc-1α enhanced levels of Drp-1 in RAECs and increased ROS generation after hypoxia, while Pgc-1α plasmid ameliorates Drp-1 expression in the presence of exogenous Thbs-1.
conclusionThese results highlight a novel signaling pathway by which Thbs-1 regulates mitochondrial fission protein (Drp-1) and ROS generation during hypoxia, and presumably, following IR. Inhibiting Thbs-1 immediately after IR may prevent Drp-1-mediated mitochondrial fission and is likely to improve the diastolic function of the heart by reducing ROS-mediated cardiomyocyte damage in the aged population.
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