ArticlePloS one2014
Gαi2- and Gαi3-deficient mice display opposite severity of myocardial ischemia reperfusion injury.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 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
23 citing papers in PubMed, 30 citations in OpenAlex.
- NLGN3 contributes to angiogenesis in myocardial infarction via activation of the Gαi1/3-Akt pathway.Basic research in cardiology · 2026Article
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- Opposite effects of GαNaunyn-Schmiedeberg's archives of pharmacology · 2025Article
- CB1 receptor coupling to extracellular regulated kinase via multiple Gαi/o isoforms.Neuroreport · 2025Article
- Targeting GαBasic research in cardiology · 2024Article
- Protective effects of GαNaunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Cerebrovascular GMolecular imaging and biology · 2023Article
- Article
- Analyses of Gnai3-iresGFP reporter mice reveal unknown GαScientific reports · 2021Article
- Lack of GαMolecular metabolism · 2020Article
- Selective protection of murine cerebral GJournal of molecular medicine (Berlin, Germany) · 2020Article
- SNHG1 Inhibits ox-LDL-Induced Inflammatory Response and Apoptosis of HUVECsFrontiers in pharmacology · 2020Article
- Ischemia/Reperfusion Injury Revisited: An Overview of the Latest Pharmacological Strategies.International journal of molecular sciences · 2019Review
- GαOncotarget · 2018Article
- RXFP1 Receptor Activation by Relaxin-2 Induces Vascular Relaxation in MiceFrontiers in physiology · 2018Article
- Defective Gpsm2/GαNature communications · 2017Article
- Regulator of G Protein Signaling 6 Protects the Heart from Ischemic Injury.The Journal of pharmacology and experimental therapeutics · 2017Article
- Knockdown of Inhibitory Guanine Nucleotide Binding Protein Giα-2 by Antisense Oligodeoxynucleotides Attenuates the Development of Hypertension and Tachycardia in Spontaneously Hypertensive Rats.Journal of the American Heart Association · 2016Article
- Lack of Gαi2 leads to dilative cardiomyopathy and increased mortality in β1-adrenoceptor overexpressing mice.Cardiovascular research · 2015Article
- Platelet Gi protein Gαi2 is an essential mediator of thrombo-inflammatory organ damage in mice.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
G-protein-coupled receptors (GPCRs) are the most abundant receptors in the heart and therefore are common targets for cardiovascular therapeutics. The activated GPCRs transduce their signals via heterotrimeric G-proteins. The four major families of G-proteins identified so far are specified through their α-subunit: Gαi, Gαs, Gαq and G12/13. Gαi-proteins have been reported to protect hearts from ischemia reperfusion injury. However, determining the individual impact of Gαi2 or Gαi3 on myocardial ischemia injury has not been clarified yet. Here, we first investigated expression of Gαi2 and Gαi3 on transcriptional level by quantitative PCR and on protein level by immunoblot analysis as well as by immunofluorescence in cardiac tissues of wild-type, Gαi2-, and Gαi3-deficient mice. Gαi2 was expressed at higher levels than Gαi3 in murine hearts, and irrespective of the isoform being knocked out we observed an up regulation of the remaining Gαi-protein. Myocardial ischemia promptly regulated cardiac mRNA and with a slight delay protein levels of both Gαi2 and Gαi3, indicating important roles for both Gαi isoforms. Furthermore, ischemia reperfusion injury in Gαi2- and Gαi3-deficient mice exhibited opposite outcomes. Whereas the absence of Gαi2 significantly increased the infarct size in the heart, the absence of Gαi3 or the concomitant upregulation of Gαi2 dramatically reduced cardiac infarction. In conclusion, we demonstrate for the first time that the genetic ablation of Gαi proteins has protective or deleterious effects on cardiac ischemia reperfusion injury depending on the isoform being absent.
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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.