“…It has also demonstrated an endocardial endothelial M Rs mediate positive inotropy in response to muscarinic agonists via activation of COX-2 [34]. Further study is needed to evaluate differences in M 3 -mAChR signaling caused by changes in receptor desensitization, sequestration [35][36][37][38][39], and up-or down-regulation and to elucidate the role of M 3 -mAChR in cardiovascular system as well in inflammation and in cancer while new findings are emerging as regards the use of cardiovascular drugs [38,55,68,69,74,75,[77][78][79]82]. M 3 -mAChR was involved in LPS-induced lung inflammation [84] and fibroblast proliferation [85] by mediating the NF-κB signaling pathway.…”