ArticlePloS one2017
Unfolded protein response plays a critical role in heart damage after myocardial ischemia/reperfusion in rats.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- Hypoxia, ROS, and HIF Signaling in I/R Injury: Implications and Future Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- The Perspective of Using Ischemic Tolerance in Clinical Practice.Biomedicines · 2026Review
- Investigation of the mechanism by which sigma-1 receptor protein mediates the IRE1-XBP-1s pathway to alleviate cerebral ischemia-reperfusion injury.European journal of medical research · 2025Article
- Endoplasmic Reticulum Stress Inhibition Promotes Mitophagy via Miro1 Reduction to Rescue Mitochondrial Dysfunction and Protect Dopamine Neurons in Parkinson's Disease.Cellular and molecular neurobiology · 2025Article
- Research progress on the natural products in the intervention of myocardial infarction.Frontiers in pharmacology · 2024Review
- Regulation of cardiac fibroblast cell death by unfolded protein response signaling.Frontiers in physiology · 2023Review
- Investigation of the effect of 8 weeks of high-intensity interval training and berberine supplementation on some echocardiography and electrocardiogram indices following myocardial ischemia-reperfusion in rats.ARYA atherosclerosis · 2022Article
- Endoplasmic reticulum as a target in cardiovascular diseases: Is there a role for flavonoids?Frontiers in pharmacology · 2022Review
- Inhibition of the unfolded protein response reduces arrhythmia risk after myocardial infarction.The Journal of clinical investigation · 2021Article
- Mutation in FBXO32 causes dilated cardiomyopathy through up-regulation of ER-stress mediated apoptosis.Communications biology · 2021Article
- The Function of KDEL Receptors as UPR Genes in Disease.International journal of molecular sciences · 2021Review
- Endoplasmic reticulum stress serves an important role in cardiac ischemia/reperfusion injury (Review).Experimental and therapeutic medicine · 2020Review
- Effect of endoplasmic reticulum stress on endothelial ischemia-reperfusion injury in humans.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Peptidylglycine α-amidating monooxygenase is required for atrial secretory granule formation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Coronary clot composition after myocardial infarction: Thrombus age matters.International journal of cardiology. Heart & vasculature · 2020Article
- Crocetin alleviates myocardial ischemia/reperfusion injury by regulating inflammation and the unfolded protein response.Molecular medicine reports · 2020Article
- Heat shock proteins and their expression in primary murine cardiac cell populations during ischemia and reperfusion.Molecular and cellular biochemistry · 2020Review
- Activation of the Unfolded Protein Response Pathway in Cytotoxic T Cells: A Comparison BetweenThe Yale journal of biology and medicine · 2019Review
- Curcumin attenuates hypoxia/reoxygenation‑induced myocardial injury.Molecular medicine reports · 2019Article
- Proteostasis and Beyond: ATF6 in Ischemic Disease.Trends in molecular medicine · 2019Review
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
The unfolded protein response (UPR) plays a critical role in cell death mediated by ischemia/reperfusion (I/R) injury. However, little is known about the exact mechanism of UPR signaling pathways after myocardial I/R injury in rats. An attempt was therefore made to assess whether the myocardial I/R induced UPR, and which branch of UPR (ATF6, IRE1 and PERK) signal pathway was activated. Sprague-Dawley rats were pretreated with UPR stimulator dithiothreitol (DTT) and UPR inhibitor 4-phenylbutyrate (4PBA) and then subjected to myocardial I/R surgery. Compared with sham-operated group, the expression of GRP78, ATF6, CHOP and sXBP1 in the I/R injured group is significantly increased at transcript and protein levels, which indicated that all the three signal pathways of UPR were activated in the myocardial I/R injury. Compared with the I/R injured group, treatment with 4PBA effectively decreased myocardium infarct size, reduced myocardial apoptosis, down-regulated caspase-12 expression, diminished serum creatine kinase and lactate dehydrogenase levels. In contrast, these effects were reversed in DTT treated group. In summary, these results demonstrated that myocardial I/R injury activates UPR and inhibiting cell UPR possesses a cardioprotective effect through the suppression of ER stress-induced apoptosis. Therefore, inhibition of UPR might be used as a therapeutic target during myocardial I/R injury.
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