I just read the first article(22), since I am on my university's network I have full access to these articles. if you want me to quote any part of it, just ask.
in the case of the first article, it speaks only about a specific situation. it's about some kind of anti-cancer drug, called DOX:
The mechanism of DOX-induced cardiotoxicity involves increased oxidative/nitrosative stress (
4–
7), matrix metalloproteinase activation (
8,
9), and alteration of cardiac energetics (
10), which eventually lead to cell death by apoptosis or cell necrosis (
11–
15). However, the exact mechanisms have not been fully established, and optimal therapeutic approaches for cardioprotection remain undefined (
3).
apparently, it has a problem though:
Doxorubicin is one of the most potent antitumor agents available; however, its clinical use is limited because of the risk of severe cardiotoxicity.
and apparently, in this case blocking the CB1-receptors(administering an antagonist, rimonabant in this study) helps against the cardiotoxicity.
I still have to read the other articles, but so far I would say it's a bit quick to make conclusions out of this for the situation not involving DOX. the first article does make some mentions in the discussion, like this:
Numerous previous experimental studies have demonstrated that activation of the endocannabinoid system may contribute to the hypotension and compromised cardiovascular function in a variety of pathophysiological states (e.g., hemorrhagic, endotoxic, and cardiogenic shock, advanced liver cirrhosis, and cirrhotic cardiomyopathy) through the activation of myocardial and vascular CB1 receptors.
but that's outside what this article discovers, I would have to look at the references to see what's behind that.
reading the 2nd article now, it's about the same situation, but it has some additional info:
In human primary cardiomyocytes expressing CB1 receptors (demonstrated by RT–PCR, western immunoblot, and flow cytometry) DOX, likewise the CB1 receptor agonist HU210 and the endocannabinoid anandamide (AEA), induced MAPK activation and cell death. The DOX-induced MAPK activation and cell death were significantly enhanced when DOX was co-administered with CB1 agonists AEA or HU210. Remarkably, cell death and MAPK activation induced by AEA, HU210, and DOX ± AEA/HU210 were largely attenuated by either CB1antagonists (rimonabant and AM281) or by inhibitors of p38 and JNK MAPKs. Furthermore, AEA or HU210 in primary human cardiomyocytes triggered increased reactive oxygen species generation.
and the conclusion:
CB1 activation in cardiomyocytes may amplify the reactive oxygen/nitrogen species-MAPK activation-cell death pathway in pathological conditions when the endocannabinoid synthetic or metabolic pathways are dysregulated by excessive inflammation and/or oxidative/nitrosative stress, which may contribute to the pathophysiology of various cardiovascular diseases.
now taking a break, but if you have any questions about what it says just ask, I realize some of these terms may be unknown for many, and while I'm not an expert either, I do recognise most terms from either my cell biology or genetics classes.
