ArticlePloS one2016
Increase in Cardiac Ischemia-Reperfusion Injuries in Opa1+/- Mouse Model.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05434481 (MITAORTA - Role of Mitochondrial Dynamic in Aneurysm and Dissection of Ascending Thoracic Aorta), which is not on this map. Cited by 39 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
MITAORTA - Role of Mitochondrial Dynamic in Aneurysm and Dissection of Ascending Thoracic Aorta
Who cites it
39 citing papers in PubMed, 65 citations in OpenAlex.
- Integrated bioinformatic and in vivo analysis confirms the cardioprotective role of OPA1.BMC cardiovascular disorders · 2025Article
- mTOR inhibition triggers mitochondrial fragmentation in cardiomyocytes through proteosome-dependent prohibitin degradation and OPA-1 cleavage.Cell communication and signaling : CCS · 2025Article
- Cardiac electrical abnormalities in a mouse model of left ventricular non-compaction cardiomyopathy.PloS one · 2025Article
- Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitors: Guardians against Mitochondrial Dysfunction and Endoplasmic Reticulum Stress in Heart Diseases.ACS pharmacology & translational science · 2024Review
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- The mitochondrial ATP synthase is a negative regulator of the mitochondrial permeability transition pore.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Targeting mitochondrial shape: at the heart of cardioprotection.Basic research in cardiology · 2023Article
- Review
- Mitochondrial dysfunction at the crossroad of cardiovascular diseases and cancer.Journal of translational medicine · 2023Review
- Mitochondrial Dysfunction in the Cardio-Renal Axis.International journal of molecular sciences · 2023Review
- Mitochondrial quality control in cardiac ischemia/reperfusion injury: new insights into mechanisms and implications.Cell biology and toxicology · 2023Review
- Mechanistic study of optic atrophy 1 in ischemia-reperfusion disease.Journal of molecular medicine (Berlin, Germany) · 2023Review
- The dynamic interplay between cardiac mitochondrial health and myocardial structural remodeling in metabolic heart disease, aging, and heart failure.The journal of cardiovascular aging · 2023Article
- Article
- The mitochondrial associated endoplasmic reticulum membranes: A platform for the pathogenesis of inflammation-mediated metabolic diseases.Immunity, inflammation and disease · 2022Review
- PEG35 as a Preconditioning Agent against Hypoxia/Reoxygenation Injury.International journal of molecular sciences · 2022Article
- Oestrogenic Regulation of Mitochondrial Dynamics.International journal of molecular sciences · 2022Review
- Mitochondrial Dynamics and Mitophagy in Cardiometabolic Disease.Frontiers in cardiovascular medicine · 2022Review
- Ischemic Preconditioning and Postconditioning Protect the Heart by Preserving the Mitochondrial Network.BioMed research international · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent data suggests the involvement of mitochondrial dynamics in cardiac ischemia/reperfusion (I/R) injuries. Whilst excessive mitochondrial fission has been described as detrimental, the role of fusion proteins in this context remains uncertain.
objectivesTo investigate whether Opa1 (protein involved in mitochondrial inner-membrane fusion) deficiency affects I/R injuries. METHODS AND
resultsWe examined mice exhibiting Opa1delTTAG mutations (Opa1+/-), showing 70% Opa1 protein expression in the myocardium as compared to their wild-type (WT) littermates. Cardiac left-ventricular systolic function assessed by means of echocardiography was observed to be similar in 3-month-old WT and Opa1+/- mice. After subjection to I/R, infarct size was significantly greater in Opa1+/- than in WTs both in vivo (43.2±4.1% vs. 28.4±3.5%, respectively; p<0.01) and ex vivo (71.1±3.2% vs. 59.6±8.5%, respectively; p<0.05). No difference was observed in the expression of other main fission/fusion protein, oxidative phosphorylation, apoptotic markers, or mitochondrial permeability transition pore (mPTP) function. Analysis of calcium transients in isolated ventricular cardiomyocytes demonstrated a lower sarcoplasmic reticulum Ca2+ uptake, whereas cytosolic Ca2+ removal from the Na+/Ca2+ exchanger (NCX) was increased, whilst SERCA2a, phospholamban, and NCX protein expression levels were unaffected in Opa1+/- compared to WT mice. Simultaneous whole-cell patch-clamp recordings of mitochondrial Ca2+ movements and ventricular action potential (AP) showed impairment of dynamic mitochondrial Ca2+ uptake and a marked increase in the AP late repolarization phase in conjunction with greater occurrence of arrhythmia in Opa1+/- mice.
conclusionOpa1 deficiency was associated with increased sensitivity to I/R, imbalance in dynamic mitochondrial Ca2+ uptake, and subsequent increase in NCX activity.
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