ArticleJournal of the American College of Cardiology2008
Aging mouse hearts are refractory to infarct size reduction with post-conditioning.
Article in Journal of the American College of Cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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Who cites it
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.
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- Constitutive activation of ERK1/2 signaling protects against myocardial ischemia via inhibition of mitochondrial fragmentation in the aging heart.Annals of translational medicine · 2021Article
- Preconditioning strategies to prevent acute kidney injury.F1000Research · 2020Review
- Cx43 phosphorylation-mediated effects on ERK and Akt protect against ischemia reperfusion injury and alter the stability of the stress-inducible protein NDRG1.The Journal of biological chemistry · 2019Article
- Ischaemic and hypoxic conditioning: potential for protection of vital organs.Experimental physiology · 2019Review
- Conditioning-induced cardioprotection: Aging as a confounding factor.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Review
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- An overview of protective strategies against ischemia/reperfusion injury: The role of hyperbaric oxygen preconditioning.Brain and behavior · 2018Review
- Repeated Remote Ischemic Conditioning Effect on Ankle-brachial Index in Diabetic Patients - A Randomized Control Trial.Advanced biomedical research · 2017Article
- Sarcolemmal dependence of cardiac protection and stress-resistance: roles in aged or diseased hearts.British journal of pharmacology · 2016Review
- Mitochondrial Metabolism in Aging Heart.Circulation research · 2016Review
- Cardiovascular KPathobiology of aging & age related diseases · 2016Review
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- Ischemic postconditioning of the isolated human myocardium: Role of the applied protocol.International journal of cardiology. Heart & vasculature · 2015Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
objectivesOur aim was to establish whether the efficacy of post-conditioning is maintained in aging hearts.
backgroundPost-conditioning, or relief of myocardial ischemia in a stuttered manner, has been shown to reduce infarct size, in part because of up-regulation of survival kinases (extracellular-signal regulated kinase [ERK] 1/2 or PI3-kinase/Akt) during the early min of reperfusion. All of these data have, however, been obtained in adult populations; the question of whether post-conditioning-induced cardioprotection is maintained in aging cohorts is unknown.
methodsIsolated buffer-perfused hearts were obtained from 3- to 4-month-old (adult) and 20- to 24-month-old C57BL/6J mice and subjected to 30 min of ischemia. For each cohort, hearts were randomized to receive standard, abrupt (control) reperfusion, or were post-conditioned with 3 or 6 10-s cycles of stuttered reflow. Primary end points were infarct size, cardiac expression of phospho-Akt, phospho-mitogen-activated protein kinase kinase 1/2 and phospho-ERK 1/2, and expression of mitogen-activated protein kinase-phosphatase-1 (MKP-1: phosphatase purported to play a primary role in ERK dephosphorylation).
resultsIn adult mouse hearts, post-conditioning significantly reduced infarct size via up-regulation of ERK (but not Akt) signaling. In contrast, in the 2-year-old cohort, post-conditioning failed to limit necrosis, possibly a consequence of the deficit in ERK phosphorylation and increased MKP-1 expression seen in old hearts. Indeed, infusion of sodium orthovanadate, a nonspecific MKP inhibitor, attenuated MKP-1 expression and restored the post-conditioned phenotype in old hearts.
conclusionsOld mouse hearts are refractory to infarct size reduction with post-conditioning, possibly because of an age-associated increase in MKP-1 and resultant deficit in ERK phosphorylation.
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