Myocardial infarction |
CB1 aggravated cardiac ischemic injuries |
CB2 mitigated cardiac ischemic injuries |
[20,23,26,27,28] |
Cardiac I/R injury |
Majority of the literature documents CB1 as a mediator of I/R injury, although there is some controversy across studies |
CB2 potently protected from I/R injury |
[29,30,31,32,33,34,35,36,37] |
Pathological cardiac hypertrophy |
Majority of the literature documents CB1 as a pro-hypertrophic receptor, and CB1 tended to be not as potent as CB2 in controlling hypertrophy |
CB2 potently conferred anti-hypertrophic property |
[38,39,40] |
Cardiac fibrosis |
CB1 promoted fibrogenesis mainly through TGF-β1/Smad3 pathway |
CB2 ameliorated cardiac fibrosis via TGFβ1-dependent and independent manners |
[23,27,29,30,40,41,42,43,44,45,46] |
Antipsychotics cardiotoxicity |
Pharmacological inhibition of CB1 was cardioprotective |
Pharmacological activation of CB2 was cardioprotective |
[47,48,49,50] |
Anti-tumor drug cardiotoxicity |
Genetic ablation or pharmacological antagonism of CB1 was cardioprotective |
Unknown |
[51,52] |
Ethanol-induced myocardial injury |
Less known |
CB2 attenuated ethanol toxicity |
[53,54] |