ArticleAmerican journal of translational research2019
Effects of GCN2/eIF2α on myocardial ischemia/hypoxia reperfusion and myocardial cells injury.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 12 citations in OpenAlex.
- A transport-independent role for SLC25A12 in mitochondrial stress signalling.Nature cell biology · 2026Article
- Article
- Sesamin Protects Against Polystyrene Microplastics-Induced Lung Injury via Attenuating Bcl2-Mediated Apoptosis.Antioxidants (Basel, Switzerland) · 2026Article
- Mammalian integrated stress responses in stressed organelles and their functions.Acta pharmacologica Sinica · 2024Review
- General Control Non-derepressible 2 Alleviates Cartilage Degeneration and Inhibits NLRP3 Inflammasome Activation in Osteoarthritis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2024Article
- General control nonderepressible 2 (GCN2) as a therapeutic target in age-related diseases.Frontiers in aging · 2024Review
- The integrated stress response in ischemic diseases.Cell death and differentiation · 2022Review
- LncRNA LINC00461 exacerbates myocardial ischemia-reperfusion injury via microRNA-185-3p/Myd88.Molecular medicine (Cambridge, Mass.) · 2022Article
- Role and Mechanism of the Renin-Angiotensin-Aldosterone System in the Onset and Development of Cardiorenal Syndrome.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2022Review
- Article
- Dexmedetomidine alleviates cardiomyocyte apoptosis and cardiac dysfunction may be associated with inhibition of RhoA/ROCK pathway in mice with myocardial infarction.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis.Molecular medicine reports · 2021Article
- GTS-21 Promotes α7 nAChR to Alleviate Intestinal Ischemia-Reperfusion-Induced Apoptosis and Inflammation of Enterocytes.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia/hypoxia-reperfusion injury is a common and severe cardiovascular disorder. General control non-derepressible 2 (GCN2) plays an important role in the role of cardiomyocyte glucose metabolism. Therefore, our study focused on the expression of GCN2/eIF2α in myocardial ischemia/hypoxia-reperfusion injury and its mechanism of myocardial cell injury. In the volunteers and patients with myocardial ischemia and hypoxia- reperfusion, the expression of GCN2 and eIF2α on serum were detected by RT-qPCR. The GCN2, eIF2α interference and GCN2 overexpression plasmids were constructed and transfected into cells. Then, the level of TNF-α, IL-1β, IL-6, IFN-γ were detected by ELISA and the level of ROS, MDA, LDH and SOD were measured by the corresponding kits, respectively. Besides, the expression of GCN2/eIF2 signaling pathway (p-eIF2α, ATF4, CHOP, UCP2 and eIF2α) and apoptosis-related proteins (Bax, Bcl-2 and cleaved caspase3) was detected by western blot. Flow cytometry was performed to value cell apoptosis. The expression of GCN2 is increased in oxygen-glucose deprivation/reoxygenation (OGD/R) model cells and GCN2 interference reduces the inflammation and oxidative stress in H9C2 cells after OGD/R. GCN2 interference reduced the level of apoptosis in OGD/R model cells and inhibited the expression of GCN2/eIF2α signaling pathway. We found that eIF2α interference could offset the effects of GCN2 overexpression on oxidative stress and apoptosis in H9C2 cells, and verified that GCN2 is produced by eIF2α phosphorylation. Together, GCN2/eIF2α signaling pathway plays an important role in myocardial ischemia/hypoxia-reperfusion injury, which could provide a new idea for the treatment of myocardial infarction on clinical.
Indexed as
Identifiers
31632531PMC6789277W2984600334What OpenQuestion holds
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.