ArticleBritish journal of pharmacology2017
Activation of G protein-coupled oestrogen receptor 1 at the onset of reperfusion protects the myocardium against ischemia/reperfusion injury by reducing mitochondrial dysfunction and mitophagy.
Article in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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
75 citing papers in PubMed, 124 citations in OpenAlex.
- Mild Hypothermia Alleviates Ischemia and Reperfusion Injury by Activating PINK1/Parkin Mitophagy.Neurochemical research · 2026Article
- Exercise-Induced Regulation of Bone Remodeling via Mitophagy: A Review of Current Evidence.Biomolecules · 2026Review
- Review
- G protein-coupled estrogen receptor GPR30 exerts vasoprotective effects in apolipoprotein E-deficient mice.Archives of medical science : AMS · 2026Article
- Mastering cardiomyocyte mitophagy: molecular governance, pathological derailment and therapeutics.PeerJ · 2026Review
- Mitophagy: a novel avenue for herbal medicines alleviating myocardial ischemia/reperfusion injury.Apoptosis : an international journal on programmed cell death · 2025Review
- GDF15 attenuates myocardial hypoxic injury by inhibiting mitochondrial damage through BNIP3 pathway.Molecular biology reports · 2025Article
- The role of estrogen in cardiac transplantation: mechanistic insights and effects on clinical outcomes.Frontiers in transplantation · 2025Review
- Mic60/Mitofilin inhibitor, Miclxin, induces rat H9C2 cardiomyoblast death by inhibiting the removal of damaged mitochondria.American journal of translational research · 2025Article
- Mitophagy in ischemic heart disease: molecular mechanisms and clinical management.Cell death & disease · 2024Review
- An update on the role of sex hormones in the function of the cardiorenal mitochondria.Biochemical Society transactions · 2024Review
- Activation of G Protein-Coupled Estrogen Receptor (GPER) Negatively Modulates Cardiac Excitation-Contraction Coupling (ECC) through the PI3K/NOS/NO Pathway.International journal of molecular sciences · 2024Article
- Prognostic factors of MINOCA and their possible mechanisms.Preventive medicine reports · 2024Review
- Cardiomyocyte peroxisome proliferator-activated receptor α prevents septic cardiomyopathy via improving mitochondrial function.Acta pharmacologica Sinica · 2023Article
- The Role of G Protein-Coupled Estrogen Receptor (GPER) in Vascular Pathology and Physiology.Biomolecules · 2023Review
- The G protein-coupled oestrogen receptor GPER in health and disease: an update.Nature reviews. Endocrinology · 2023Review
- Salvianolic Acid B Inhibits Ferroptosis and Apoptosis during Myocardial Ischemia/Reperfusion Injury via Decreasing the Ubiquitin-Proteasome Degradation of GPX4 and the ROS-JNK/MAPK Pathways.Molecules (Basel, Switzerland) · 2023Article
- Mitophagy as a mitochondrial quality control mechanism in myocardial ischemic stress: from bench to bedside.Cell stress & chaperones · 2023Review
- Mitofilin Heterozygote Mice Display an Increase in Myocardial Injury and Inflammation after Ischemia/Reperfusion.Antioxidants (Basel, Switzerland) · 2023Article
- Heart Failure in Menopause: Treatment and New Approaches.International journal of molecular sciences · 2022Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 3 countries.
Funding
Abstract
background and purposeRecent evidence indicates that GPER (G protein-coupled oestrogen receptor 1) mediates acute pre-ischaemic oestrogen-induced protection of the myocardium from ischaemia/reperfusion injury via a signalling cascade that includes PKC translocation, ERK1/2/ GSK-3β phosphorylation and inhibition of the mitochondrial permeability transition pore (mPTP) opening. Here, we investigated the impact and mechanism involved in post-ischaemic GPER activation in ischaemia/reperfusion injury. We determined whether GPER activation at the onset of reperfusion confers cardioprotective effects by protecting against mitochondrial impairment and mitophagy. EXPERIMENTAL APPROACH: In vivo rat hearts were subjected to ischaemia followed by reperfusion with oestrogen (17β-oestradiol, E2), E2 + G15, a GPER antagonist, or vehicle. Myocardial infarct size, the threshold for the opening of mPTP, mitophagy, mitochondrial membrane potential, ROS production, proteins ubiquitinated including cyclophilin D, and phosphorylation levels of ERK and GSK-3β were measured.
resultsWe found that post-ischaemic E2 administration to both male and female ovariectomized-rats reduced myocardial infarct size. Post-ischaemic E2 administration preserved mitochondrial structural integrity and this was associated with a decrease in ROS production and increased mitochondrial membrane potential, as well as an increase in the mitochondrial Ca
conclusionThese results indicate that post-ischaemic GPER activation induces cardioprotective effects against ischaemia/reperfusion injury in males and females by protecting mitochondrial structural integrity and function and reducing 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.