ArticleMolecular and cellular biochemistry2005
Signal transduction mechanisms involved in cardiac preconditioning: role of Ras-GTPase, Ca2+/calmodulin-dependent protein kinase II and epidermal growth factor receptor.
Article in Molecular and cellular biochemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 38 citations in OpenAlex.
- Review
- The cardiac toxicity of PAMAM dendrimer drug delivery systems can be attenuated with the adjunct use of cardioprotective agents.Biomolecules & biomedicine · 2025Article
- Mitigating Cardiotoxicity of Dendrimers: Angiotensin-(1-7) via Its Mas Receptor Ameliorates PAMAM-Induced Cardiac Dysfunction in the Isolated Mammalian Heart.Pharmaceutics · 2022Article
- Flavonoids in myocardial ischemia-reperfusion injury: Therapeutic effects and mechanisms.Chinese herbal medicines · 2021Review
- The Role of Epidermal Growth Factor Receptor Family of Receptor Tyrosine Kinases in Mediating Diabetes-Induced Cardiovascular Complications.Frontiers in pharmacology · 2021Review
- Nanotoxicology of Dendrimers in the Mammalian Heart: ex vivo and in vivo Administration of G6 PAMAM Nanoparticles Impairs Recovery of Cardiac Function Following Ischemia-Reperfusion Injury.International journal of nanomedicine · 2020Article
- Cardioprotection of ischaemic preconditioning is associated with inhibition of translocation of MLKL within the plasma membrane.Journal of cellular and molecular medicine · 2018Article
- Epidermal Growth Factor Receptor Transactivation: Mechanisms, Pathophysiology, and Potential Therapies in the Cardiovascular System.Annual review of pharmacology and toxicology · 2016Article
- Diabetic cardiomyopathy: Role of epidermal growth factor receptor tyrosine kinase.Journal of molecular and cellular cardiology · 2015Article
- CaMKII-dependent responses to ischemia and reperfusion challenges in the heart.Frontiers in pharmacology · 2014Review
- The role of epidermal growth factor receptor in diabetes-induced cardiac dysfunction.BioImpacts : BI · 2013Article
- Molecular alterations associated with the NMDA preconditioning-induced neuroprotective mechanism against glutamate cytotoxicity.Journal of molecular neuroscience : MN · 2012Article
- Article
- Protein Kinases as Drug Development Targets for Heart Disease Therapy.Pharmaceuticals (Basel, Switzerland) · 2010Review
- Activation of a novel estrogen receptor, GPER, is cardioprotective in male and female rats.American journal of physiology. Heart and circulatory physiology · 2009Article
- Regulation of two-pore-domain (K2P) potassium leak channels by the tyrosine kinase inhibitor genistein.British journal of pharmacology · 2008Article
- Increased O-GlcNAc levels during reperfusion lead to improved functional recovery and reduced calpain proteolysis.American journal of physiology. Heart and circulatory physiology · 2007Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well established that brief episodes of ischemia/reperfusion (I/R) [preconditioning (PC)] protect the myocardium from the damage induced by subsequent more prolonged I/R. However, the signaling pathways activated during PC or I/R are not well characterized. In this study, the role of Ras-GTPase, tyrosine kinases (TKs), epidermal growth factor receptor (EGFR) and Ca2+/calmodulin-dependent protein kinase II (CaMK II) in mediating PC in a perfused rat heart model was investigated. A 40-min episode of global ischemia in perfused rat hearts produced significantly impaired cardiac function, measured as left ventricular developed pressure (Pmax) and left ventricular end-diastolic pressure (LVEDP), and impaired coronary hemodynamics, measured as coronary flow (CF) and coronary vascular resistance (CVR). PC significantly enhanced cardiac recovery after IR. Combination of PC and FPT III (Ras-GTPase inhibitor FPT III; 232 ng/min for 6 days) treatment did not produce any additive benefits as compared to PC alone. In contrast, PC-induced improvements in cardiac function after I/R were significantly attenuated by pretreatment with genistein (1mg/kg/day for 6 days), a broad-spectrum inhibitor of TKs, or AG1478 (1mg/kg/day for 6 days), a specific inhibitor of EGFR tyrosine kinase or KN-93 (578 ng/min for 6 days), a CaMK II inhibitor, before PC. These observations suggest that PC and FPT III pretreatment may produce cardioprotection via similar mechanisms. Present results also indicate that activation of TKs and specifically activation of EGFR-mediated TKs and CaMK II-mediated regulation of calcium homeostasis are part of the PC mechanisms that improve recovery after IR.
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