Regular ArticleAttenuation of Myocardial Ischaemic Injury 24 h After Diacylglycerol TreatmentIn Vivo☆
References (0)
Cited by (24)
Lipid partitioning during cardiac stress
2016, Biochimica et Biophysica Acta - Molecular and Cell Biology of LipidsCitation Excerpt :DAGs are a notorious activator of PKC signaling and PKC activation, primarily the PKCϵ isoform, has been implicated in cardioprotection from ischemia [104–106]. DAG analogs have been given in experimental I–R with some success [107,108]. From these limited studies, it remains to be seen whether the potential increase in DAG content during ischemia is beneficial or detrimental.
Intracellular diglycerides in relation to glycaemic control in the myocardium: A pilot study in humans
2015, Diabetes and MetabolismCitation Excerpt :Specifically to the myocardium, intracellular diglyceride pool may possess significant cardio-protective functions. For example, animal studies have found that diglycerides may be involved in ameliorating the myocardial dysfunction in streptozotocin-induced diabetes [8], or reduce infarcts size during ischemia-reperfusion injury [9,10]. To our best knowledge, no direct measurements of myocardial diglycerides in humans have ever been presented.
Intermittent hypoxia-induced delayed cardioprotection is mediated by PKC and triggered by p38 MAP kinase and Erk1/2
2007, Journal of Molecular and Cellular CardiologyCitation Excerpt :We showed that IH-induced cardioprotection was abolished when chelerythrine was infused before ischemia. This is in accordance with other studies which have shown, using chelerythrine, a role for PKC in mediating delayed ischemic [13] and pharmacological [26] PC. However, the implication of other kinases cannot be excluded since chelerythrine has been reported to affect some of them [27].
Pharmacological modulation, preclinical studies, and new clinical features of myocardial ischemic preconditioning
2000, Pharmacology and TherapeuticsModulation of neutrophil migration and superoxide anion release by metoprolol
2000, Journal of Molecular and Cellular Cardiology
- ☆
Please address all correspondence to: D. M. Yellon, The Hatter Institute for Cardiovascular Studies, Division of Cardiology, University College London Hospital & Medical School, Grafton Way, London WC1E 6DB, UK.