ArticleJournal of geriatric cardiology : JGC2018
C-reactive protein aggravates myocardial ischemia/reperfusion injury through activation of extracellular-signal-regulated kinase 1/2.
Article in Journal of geriatric cardiology : JGC, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Predictive Value of High-Sensitivity CRP Level on the No-Reflow Phenomenon in STEMI Patients.Cardiology research and practice · 2025Article
- Oleuropein alleviates myocardial ischemia-reperfusion injury by suppressing oxidative stress and excessive autophagy via TLR4/MAPK signaling pathway.Chinese medicine · 2024Article
- Mitochondrial Damage in Myocardial Ischemia/Reperfusion Injury and Application of Natural Plant Products.Oxidative medicine and cellular longevity · 2022Review
- Mitochondrial DNA Efflux Maintained in Gingival Fibroblasts of Patients with Periodontitis through ROS/mPTP Pathway.Oxidative medicine and cellular longevity · 2022Article
- Detrimental Effect of C-Reactive Protein on the Cardiometabolic Cells and Its Rectifying by Metabolic Surgery in Obese Diabetic Patients.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Long noncoding RNA FTX ameliorates hydrogen peroxide-induced cardiomyocyte injury by regulating the miR-150/KLF13 axis.Open life sciences · 2020Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemia/reperfusion injury (IRI) is an inflammatory response that occurs when tissue is reperfused following a prolonged period of ischemia. Several studies have indicated that C-reactive protein (CRP) might play an important role in inducing IRI. However, the effects of CRP on myocardial IRI and the underlying mechanisms have not been fully elucidated. This study aimed to investigate the association between CRP and myocardial IRI and the underlying mechanisms.
methodsWe simulated ischemia/reperfusion using oxygen-glucose deprivation/ reoxygenation (OGD/R) in neonatal Sprague-Dawley rat cardiomyocytes; reperfusion injury was induced by three hours of hypoxia with glucose and serum deprivation followed by one hour of reperfusion. Cell viability was tested with MTS assays, and cardiomyocyte damage was evaluated by lactate dehydrogenase (LDH) leakage. Mitochondrial membrane potential was measured using tetramethylrhodamine ethyl ester (TMRE) and mitochondrial permeability transition pore (mPTP) opening was measured using calcein/AM; both TMRE and caocein/AM were visualized with laser scanning confocal microscopy. In addition, we studied the signaling pathways underlying CRP-mediated ischemia/reperfusion injury via Western blot analysis.
resultsCompared with the simple OGD/R group, after intervention with 10 µg/mL CRP, cell viability decreased markedly (82.36 % ± 6.18%
conclusionsOur results suggested that CRP directly aggravates myocardial IRI in myocardial cells and that this effect is primarily mediated by inhibiting mitochondrial ATP-sensitive potassium (mitoK
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