ArticleHeart and vessels2011
Study on the relationship of cPLA2, CK-MB, and membrane phospholipid content in acute myocardial infarction.
Article in Heart and vessels, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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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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.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- The predictive value of CK-MB on the curative effect of urokinase combined with LMWH calcium in AMI.Biomarkers in medicine · 2024Trial
- Window current through the T-type Ca2+ channel triggers the mechanism for cellular apoptosis via mitochondrial pathways.Heart and vessels · 2013Article
- Sulfur dioxide inhibits excessively activated endoplasmic reticulum stress in rats with myocardial injury.Heart and vessels · 2012Article
- Bio-tea prevents membrane destabilization during Isoproterenol-induced myocardial injury.Journal of microscopy and ultrastructureArticle
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased plasma creatine kinase-myoglobin (CK-MB) occurs in patients with acute myocardial infarction (AMI), but its underlying relationship with cytosolic phospholipase A2 (cPLA2) is poorly understood. In the present study we sought to determine cPLA2 activation and its relationship with plasma and myocardial CK-MB level and membrane phospholipids (PLs) in an animal model of AMI. AMI was induced in 60 male Sprague-Dawley rats by ligating the left anterior descending of coronary artery. Rats were randomized into six groups at 0 (sham group), 1, 2, 4, 6, and 12 h after AMI onset (ten rats in each group). cPLA2 was detected by reverse transcription polymerase chain reaction and immunohistochemical staining for mRNA and protein expression, respectively. Plasma and myocardial CK-MB activity were measured by inhibition kinetics, and membrane PLs were determined by phosphorus quantitative method. Myocardial cPLA2 expression increased from 1 h and reached a peak at 2 h after AMI onset (p < 0.01) followed by a decrease but still remained high, whereas plasma CK-MB significantly increased in rats from 4 h after the onset of AMI (p < 0.05). During the first 6 h of AMI, a negative correlation existed between myocardial cPLA2 and membrane PLs (r = -0.504, p < 0.01), whereas myocardial cPLA2 levels were positively associated with plasma CK-MB (r = 0.741, p < 0.01) but negatively correlated with myocardial CK-MB in AMI groups (r = -0.785, p < 0.01). Myocardial cPLA2 level increased and is positively correlated with plasma CK-MB activity and negatively correlated with membrane phospholipid content in AMI rats at early stage.
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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.