ArticleClinical and translational science2011
Cytosolic phospholipase A(2)α protects against ischemia/reperfusion injury in the heart.
Article in Clinical and translational science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Drug Signature-based Finding of Additional Clinical Use of LC28-0126 for Neutrophilic Bronchial Asthma.Scientific reports · 2015Trial
- The Link between Prostanoids and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Omega-3 fatty acid prevents the development of heart failure by changing fatty acid composition in the heart.Scientific reports · 2020Article
- Modeling Membrane Curvature Generation due to Membrane⁻Protein Interactions.Biomolecules · 2018Review
- Chronic intermittent hypoxia affects the cytosolic phospholipase AMolecular and cellular biochemistry · 2016Article
- Differential activation of cultured neonatal cardiomyocytes by plasmalemmal versus intracellular G protein-coupled receptor 55.The Journal of biological chemistry · 2013Article
- The absence of myocardial calcium-independent phospholipase A2γ results in impaired prostaglandin E2 production and decreased survival in mice with acute Trypanosoma cruzi infection.Infection and immunity · 2013Article
- The molecular basis of ceramide-1-phosphate recognition by C2 domains.Journal of lipid research · 2013Article
- C2 domain membrane penetration by group IVA cytosolic phospholipase A₂ induces membrane curvature changes.Journal of lipid research · 2012Article
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
Studies with sPLA(2) Group X, and cPLA(2) α gene-targeted mice suggest that absence of sPLA(2) Group X results in protection from ischemia/reperfusion (I/R) injury in the heart, and absence of cPLA(2) α Group IV is protective in the brain. Although latter studies might suggest a similar deleterious role for cPLA(2) α in I/R injury in the heart, the pathophysiology of stroke is intricately related to excitotoxicity and cannot necessarily be extrapolated to the heart. We report here that unlike findings in the brain, cPLA(2) α((-/-)) mice have exaggerated injury following I/R in vivo. In contrast, there is no difference in injury induced by simulated ischemia in cardiomyocytes isolated from cPLA(2) α((-/-)) versus cPLA(2) α((+/+)) mice. This suggests that cPLA(2) α does not have an important cardiomyocyte autonomous effect on ischemic injury. Prostaglandin E(2) (PGE(2) ) levels are significantly reduced in the hearts of the cPLA(2) α((-/-)) mice, and the enhanced injury is ameliorated by treatment with the PGE analog, misoprostol. We demonstrate that cPLA(2) α is cardioprotective in vivo, and this is likely via cPLA(2) α-mediated production of cardioprotective eicosanoids. These studies are the first to identify a protective role for cPLA(2) in I/R injury in any organ and raise concerns over long-term inhibition of cPLA(2).
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Registered trials
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