ArticleJournal of molecular and cellular cardiology2007
Impaired p38 MAPK/HSP27 signaling underlies aging-related failure in opioid-mediated cardioprotection.
Article in Journal of molecular and cellular cardiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 71 citations in OpenAlex.
- Exercise-induced cardioprotection: From endogenous to exogenous mechanisms.Sports medicine and health science · 2025Review
- Characterization of an in vitro 3D intestinal organoid model by using massive RNAseq-based transcriptome profiling.Scientific reports · 2021Article
- Could Small Heat Shock Protein HSP27 Be a First-Line Target for Preventing Protein Aggregation in Parkinson's Disease?International journal of molecular sciences · 2021Review
- Morphine induces physiological, structural, and molecular benefits in the diabetic myocardium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse.International journal of molecular sciences · 2020Review
- p38-Regulated/activated protein kinase plays a pivotal role in protecting heart against ischemia-reperfusion injury and preserving cardiac performance.American journal of physiology. Cell physiology · 2019Article
- Helium-Induced Changes in Circulating Caveolin in Mice Suggest a Novel Mechanism of Cardiac Protection.International journal of molecular sciences · 2019Article
- Exosomes from adipose-derived mesenchymal stem cells prevent cardiomyocyte apoptosis induced by oxidative stress.Cell death discovery · 2019Article
- Transcriptional regulation of stress kinase JNK2 in pro-arrhythmic CaMKIIδ expression in the aged atrium.Cardiovascular research · 2018Article
- Caveolins as Regulators of Stress Adaptation.Molecular pharmacology · 2018Review
- Stress Signaling JNK2 Crosstalk With CaMKII Underlies Enhanced Atrial Arrhythmogenesis.Circulation research · 2018Article
- The stress kinase JNK regulates gap junction Cx43 gene expression and promotes atrial fibrillation in the aged heart.Journal of molecular and cellular cardiology · 2018Article
- Sarcolemmal dependence of cardiac protection and stress-resistance: roles in aged or diseased hearts.British journal of pharmacology · 2016Review
- Mitochondria in the middle: exercise preconditioning protection of striated muscle.The Journal of physiology · 2016Review
- Prospects for Creation of Cardioprotective and Antiarrhythmic Drugs Based on Opioid Receptor Agonists.Medicinal research reviews · 2016Review
- Molecular Pharmacology of δ-Opioid Receptors.Pharmacological reviews · 2016Review
- Caveolins in cardioprotection - translatability and mechanisms.British journal of pharmacology · 2015Review
- Opioid receptors and cardioprotection - 'opioidergic conditioning' of the heart.British journal of pharmacology · 2015Review
- Article
- Sarcolemmal cholesterol and caveolin-3 dependence of cardiac function, ischemic tolerance, and opioidergic cardioprotection.American journal of physiology. Heart and circulatory physiology · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Cardioprotection and preconditioning mediated via G-protein-coupled receptors may be lost or impaired with advancing age, limiting ischemic tolerance and the ability to pharmacologically protect older hearts from ischemic injury. Our preliminary findings indicated a loss of delta-opioid receptor-mediated protection in aged vs. young mouse hearts, which may involve alterations in protective kinase signaling. In the present study, we tested the hypothesis that aging-related loss of opioid-triggered cardioprotection involves failure to activate p38 MAPK and its distal signaling targets. Langendorff-perfused hearts from young (10-14 weeks) or aged (24-26 months) C57 mice underwent 25-min ischemia and 45-min reperfusion in the presence or absence of 1 micromol/l DPDPE (delta-opioid agonist) or 1 micromol/l anisomycin (activator of p38 MAPK), and functional recovery and protein activation/phosphorylation were assessed. Contractile recovery was similar in untreated young and aged hearts (50+/-2% and 53+/-5%, respectively), and was enhanced by DPDPE in young hearts only (67+/-3%). Immunoblot analysis revealed that DPDPE comparably activated or phosphorylated GRK2, Akt, ERK1/2 and p70S6 kinase in young and aged hearts, whereas aging abrogated the stimulatory effects of DPDPE on p38 MAPK and HSP27. Treatment with anisomycin elicited comparable activation of p38 MAPK and HSP27 in both young and aged hearts, coupled with a pronounced and equivalent cardioprotection in the two groups (73+/-3% and 77+/-2%, respectively), an effect abolished by the p38 MAPK inhibitor, SB203580. These data indicate that aging-related loss of delta-opioid-mediated cardioprotection involves failure to activate p38 MAPK and HSP27. Direct targeting of this pathway elicits comparable protection in both age groups.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.