ArticleBioengineered2022
Mitophagy alleviates ischemia/reperfusion-induced microvascular damage through improving mitochondrial quality control.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Bibliometric analysis of research hotspots and emerging trends in mitophagy and atherosclerosis (2004-2024).Frontiers in medicine · 2025Pooled it
- Mitochondrial protection role of oxidoreductase-like domain containing 1 in myocardial cells under hypoxia.Medical gas research · 2026Article
- Mitophagy in Brain Injuries: Mechanisms, Roles, and Therapeutic Potential.Molecular neurobiology · 2025Review
- c-FLIP Protects Cardiac Microcirculation in Sepsis-Induced Myocardial Dysfunction Via FUNDC1-Mediated Regulation of Mitochondrial Autophagy.JACC. Basic to translational science · 2025Article
- Decoding interaction between mitochondria and endoplasmic reticulum in ischemic myocardial injury: targeting natural medicines.Frontiers in pharmacology · 2025Review
- The multifaceted role of mitochondria in cardiac function: insights and approaches.Cell communication and signaling : CCS · 2024Review
- The Role of Endothelial Cell Mitophagy in Age-Related Cardiovascular Diseases.Aging and disease · 2024Review
- Renal aging and mitochondrial quality control.Biogerontology · 2024Review
- Review
- Transcriptomic Analysis of Cardiac Tissues in a Rodent Model of Coronary Microembolization.Journal of inflammation research · 2024Article
- Article
- The role and mechanisms of microvascular damage in the ischemic myocardium.Cellular and molecular life sciences : CMLS · 2023Review
- The Current State of Research on Sirtuin-Mediated Autophagy in Cardiovascular Diseases.Journal of cardiovascular development and disease · 2023Review
- Article
- IDH2 Deficiency Promotes Endothelial Senescence by Eliciting miR-34b/c-Mediated Suppression of Mitophagy and Increased ROS Production.Antioxidants (Basel, Switzerland) · 2023Article
- Myocardial injury: where inflammation and autophagy meet.Burns & trauma · 2023Review
- Mitophagy in atherosclerosis: from mechanism to therapy.Frontiers in immunology · 2023Review
- Review
- Identification of the metabolic remodeling profile in the early-stage of myocardial ischemia and the contributory role of mitochondrion.Bioengineered · 2022Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The coronary arteries mainly function to perfuse the myocardium. When coronary artery resistance increases, myocardial perfusion decreases and myocardial remodeling occurs. Mitochondrial damage has been regarded as the primary cause of microvascular dysfunction. In the present study, we explored the effects of mitophagy activation on microvascular damage. Hypoxia/reoxygenation injury induced mitochondrial oxidative stress, thereby promoting mitochondrial dysfunction in endothelial cells. Mitochondrial impairment induced apoptosis, reducing the viability and proliferation of endothelial cells. However, supplementation with the mitophagy inducer urolithin A (UA) preserved mitochondrial function by reducing mitochondrial oxidative stress and stabilizing the mitochondrial membrane potential in endothelial cells. UA also sustained the viability and improved the proliferative capacity of endothelial cells by suppressing apoptotic factors and upregulating cyclins D and E. In addition, UA inhibited mitochondrial fission and restored mitochondrial fusion, which reduced the proportion of fragmented mitochondria within endothelial cells. UA enhanced mitochondrial biogenesis in endothelial cells by upregulating sirtuin 3 and peroxisome proliferator-activated receptor gamma coactivator 1-alpha. These results suggested that activation of mitophagy may reduce hypoxia/reoxygenation-induced cardiac microvascular damage by improving mitochondrial quality control and increasing cell viability and proliferation.
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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.