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Targeting the endocannabinod system to limit myocardial and cerebral ischemic and reperfusion injury.
Curr Pharm Biotechnol 2012; 13(1):46-58CP

Abstract

Coronary and carotid arterial occlusion due to thrombosis after atherosclerotic plaque rupture is the major cause of myocardial and cerebral infarction. Together these acute events represent the leading cause of death worldwide. Early reperfusion is the best method to salvage the ischemic organ; however, it leads to additional damage known as reperfusion injury. A large number of experimental studies has been performed in the past aimed at targeting individual mediators of reperfusion injury such as treatment with anti-oxidants or anti-inflammatory agents. Although many agents proved beneficial in animal models of myocardial or cerebral ischemia/reperfusion, the attempts to translate these protective effects into clinical practice were mostly disappointing. Elucidating the complex cellular and molecular mechanisms involved in ischemic cell death is crucial for the development of more efficient drugs in order to improve current treatment strategies. The aim of this review is to discuss cannabinoid and endocannabinoid-mediated effects in the pathogenesis of myocardial infarction and reperfusion injury, post-myocardial infarction remodeling, as well as ischemic stroke and reperfusion injury. We report experimental evidence suggesting that targeting the endocannabinoid system might evolve as a novel therapeutic concept to limit the devastating consequences of these acute vascular events through a wide variety of mechanisms, including lowering inflammation, oxidative stress, fibrosis, and excitotoxicity, and enhanced blood flow.

Authors+Show Affiliations

Center for Substance Abuse Research and Department of Physiology, Temple University, School of Medicine, Philadelphia, PA, USA.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

21470162

Citation

Tuma, Ronald F., and Sabine Steffens. "Targeting the Endocannabinod System to Limit Myocardial and Cerebral Ischemic and Reperfusion Injury." Current Pharmaceutical Biotechnology, vol. 13, no. 1, 2012, pp. 46-58.
Tuma RF, Steffens S. Targeting the endocannabinod system to limit myocardial and cerebral ischemic and reperfusion injury. Curr Pharm Biotechnol. 2012;13(1):46-58.
Tuma, R. F., & Steffens, S. (2012). Targeting the endocannabinod system to limit myocardial and cerebral ischemic and reperfusion injury. Current Pharmaceutical Biotechnology, 13(1), pp. 46-58.
Tuma RF, Steffens S. Targeting the Endocannabinod System to Limit Myocardial and Cerebral Ischemic and Reperfusion Injury. Curr Pharm Biotechnol. 2012;13(1):46-58. PubMed PMID: 21470162.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Targeting the endocannabinod system to limit myocardial and cerebral ischemic and reperfusion injury. AU - Tuma,Ronald F, AU - Steffens,Sabine, PY - 2010/05/26/received PY - 2010/08/03/accepted PY - 2011/4/8/entrez PY - 2011/4/8/pubmed PY - 2012/5/30/medline SP - 46 EP - 58 JF - Current pharmaceutical biotechnology JO - Curr Pharm Biotechnol VL - 13 IS - 1 N2 - Coronary and carotid arterial occlusion due to thrombosis after atherosclerotic plaque rupture is the major cause of myocardial and cerebral infarction. Together these acute events represent the leading cause of death worldwide. Early reperfusion is the best method to salvage the ischemic organ; however, it leads to additional damage known as reperfusion injury. A large number of experimental studies has been performed in the past aimed at targeting individual mediators of reperfusion injury such as treatment with anti-oxidants or anti-inflammatory agents. Although many agents proved beneficial in animal models of myocardial or cerebral ischemia/reperfusion, the attempts to translate these protective effects into clinical practice were mostly disappointing. Elucidating the complex cellular and molecular mechanisms involved in ischemic cell death is crucial for the development of more efficient drugs in order to improve current treatment strategies. The aim of this review is to discuss cannabinoid and endocannabinoid-mediated effects in the pathogenesis of myocardial infarction and reperfusion injury, post-myocardial infarction remodeling, as well as ischemic stroke and reperfusion injury. We report experimental evidence suggesting that targeting the endocannabinoid system might evolve as a novel therapeutic concept to limit the devastating consequences of these acute vascular events through a wide variety of mechanisms, including lowering inflammation, oxidative stress, fibrosis, and excitotoxicity, and enhanced blood flow. SN - 1873-4316 UR - https://www.unboundmedicine.com/medline/citation/21470162/abstract/Targeting_the_Endocannabinod_System_to_Limit_Myocardial_and_Cerebral_Ischemic_and_Reperfusion_Injury_ L2 - http://www.eurekaselect.com/76055/article DB - PRIME DP - Unbound Medicine ER -