Key result
Post-conditioning reduces infarct size in adult but not aged mice, linked to ERK phosphorylation deficits.
Why the study?
Post-conditioning reduces infarct size in adult populations, but whether this cardioprotection is maintained in aging hearts was unknown.
RCT
randomized
No takes yet. Share an insight, caveat, or question.
Randomized preclinical study demonstrates lack of cardioprotection from post-conditioning in aging mouse hearts, suggesting phosphatase-mediated blunting of survival kinase pathways.
Przyklenk et al. (2008) conducted an RCT in Myocardial ischemia. Post-conditioning vs. Standard, abrupt (control) reperfusion was evaluated on Infarct size, cardiac expression of phospho-Akt, phospho-mitogen-activated protein kinase kinase 1/2 and phospho-ERK 1/2, and expression of MKP-1. Post-conditioning significantly reduced infarct size in adult mouse hearts but failed to limit necrosis in 2-year-old mouse hearts, possibly due to a deficit in ERK phosphorylation.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: