“Post-myocardial infarction (MI) heart failure is a major public health problem in Western countries and results from ischemia/reperfusion (IR)-induced cell death, remodeling, and contractile dysfunction.
Ex vivo studies have demonstrated the cardioprotective anti-inflammatory effect of the cannabinoid type 2 (CB2) receptor agonists within hours after IR.
Herein, we evaluated the in vivo effect of CB2 receptors on IR-induced cell death, fibrosis, and cardiac dysfunction and investigated the target role of cardiac myocytes and fibroblasts… CB2 receptor activation may protect against post-IR heart failure through direct inhibition of cardiac myocyte and fibroblast death and prevention of myofibroblast activation…
In conclusion, modulation of the endocannabinoid system is emerging as a novel approach for the therapy of various inflammatory, metabolic, cardiovascular, hepatic, and neurodegenerative disorders.
CB1 receptors exert cardioprotective effects in cirrhotic rats and against doxorubicin toxicity. Pharmacological inhibition of the endocannabinoid degradative pathway, fatty acid aminohydrolase, represents a novel protective strategy against chronic inflammation, oxidative and nitrative stresses, and apoptosis associated with cardiovascular aging and atherosclerosis.
CB2 receptor activation is thought to be anti-inflammatory and involved in protective mechanisms during atherosclerosis. In addition, selective CB2 agonists protect against cerebral and hepatic IR injuries.
We demonstrated a highly protective role of CB2 receptors in post-IR cardiac remodeling, potentially related to activation of antiapoptotic, prosurvival, and antifibrogenic pathways.
Our results infer that CB2 agonists may be useful in preventing reperfusion injury in acute coronary syndrome and provide novel evidence for the pivotal role of CB2 receptors in post-IR-induced cardiomyopathy.”