Key result
Administration of the A2AR agonist ATL146e significantly reduced infarct size and T-cell accumulation in mice, an effect primarily mediated by inhibition of CD4+ T-cell accumulation and activation.
Why the study?
Does A2AR activation reduce infarct size in myocardial ischemia/reperfusion injury via effects on CD4+ T lymphocytes?
Does A2AR activation reduce infarct size in myocardial ischemia/reperfusion injury via effects on CD4+ T lymphocytes?
The infarct-sparing effect of adenosine A2A receptor activation during reperfusion is primarily mediated by the inhibition of CD4+ T-cell accumulation and activation.
No takes yet. Share an insight, caveat, or question.
May support A2AR agonists to limit reperfusion injury; leaves open translation from mice to patients.
Yang et al. (2006) studied Myocardial ischemia/reperfusion injury. A2AR agonist ATL146e vs. Control (implied, vehicle or different KO models) was evaluated on Infarct size (percentage of risk area) and T-cell accumulation. Administration of the A2AR agonist ATL146e significantly reduced infarct size and T-cell accumulation in mice, an effect primarily mediated by inhibition of CD4+ T-cell accumulation and activation.
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