ReviewOxidative medicine and cellular longevity2016
The Role of Mitochondrial Functional Proteins in ROS Production in Ischemic Heart Diseases.
Review in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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Who cites it
26 citing papers in PubMed, 54 citations in OpenAlex.
- SGLT2 Inhibitors in Hypertrophic Cardiomyopathy: Emerging Evidence and Putative Mechanisms.Biomolecules · 2026Review
- Enhanced Mitochondrial Dynamics and Reactive Oxygen Species Levels with Reduced Antioxidant Defenses in Human Epicardial Adipose Tissue.Metabolites · 2025Article
- Review
- HAntioxidants (Basel, Switzerland) · 2023Review
- Nrf2 protects against myocardial ischemia-reperfusion injury in diabetic rats by inhibiting Drp1-mediated mitochondrial fission.Open medicine (Warsaw, Poland) · 2023Article
- Modulating mitochondrial dynamics attenuates cardiac ischemia-reperfusion injury in prediabetic rats.Acta pharmacologica Sinica · 2022Article
- Fluorescent probes for visualizing ROS-associated proteins in disease.Chemical science · 2021Review
- Current Updates on Potential Role of Flavonoids in Hypoxia/Reoxygenation Cardiac Injury Model.Cardiovascular toxicology · 2021Review
- Review
- Mitophagy in Human Diseases.International journal of molecular sciences · 2021Review
- Melanocortin 1 receptor attenuates early brain injury following subarachnoid hemorrhage by controlling mitochondrial metabolismTheranostics · 2021Article
- Role of PI3-Kinase in Angiotensin II-Induced Cardiac Hypertrophy: Class I Versus Class III.Frontiers in pharmacology · 2021Article
- Nlrp3 Deficiency Alleviates Angiotensin II-Induced Cardiomyopathy by Inhibiting Mitochondrial Dysfunction.Oxidative medicine and cellular longevity · 2021Article
- Melatonin alleviates angiotensin-II-induced cardiac hypertrophy via activating MICU1 pathway.Aging · 2020Article
- SIRT1/SIRT3 Modulates Redox Homeostasis during Ischemia/Reperfusion in the Aging Heart.Antioxidants (Basel, Switzerland) · 2020Review
- Dexmedetomidine Protects against Myocardial Ischemia/Reperfusion Injury by Ameliorating Oxidative Stress and Cell Apoptosis through the Trx1-Dependent Akt Pathway.BioMed research international · 2020Article
- Capsaicin Alleviates the Deteriorative Mitochondrial Function by Upregulating 14-3-3Oxidative medicine and cellular longevity · 2020Article
- Sirtuin1 Role in the Melatonin Protective Effects Against Obesity-Related Heart Injury.Frontiers in physiology · 2020Article
- Hypertrophic Cardiomyopathy: A Vicious Cycle Triggered by Sarcomere Mutations and Secondary Disease Hits.Antioxidants & redox signaling · 2019Review
- Mitochondrial Dynamics in Rat Heart Induced by 5-Fluorouracil.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic heart diseases (IHD) have become the leading cause of death around the world, killing more than 7 million people annually. In IHD, the blockage of coronary vessels will cause irreversible cell injury and even death. As the "powerhouse" and "apoptosis center" in cardiomyocytes, mitochondria play critical roles in IHD. Ischemia insult can reduce myocardial ATP content, resulting in energy stress and overproduction of reactive oxygen species (ROS). Thus, mitochondrial abnormality has been identified as a hallmark of multiple cardiovascular disorders. To date, many studies have suggested that these mitochondrial proteins, such as electron transport chain (ETC) complexes, uncoupling proteins (UCPs), mitochondrial dynamic proteins, translocases of outer membrane (Tom) complex, and mitochondrial permeability transition pore (MPTP), can directly or indirectly influence mitochondria-originated ROS production, consequently determining the degree of mitochondrial dysfunction and myocardial impairment. Here, the focus of this review is to summarize the present understanding of the relationship between some mitochondrial functional proteins and ROS production in IHD.
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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.