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The ratio of infarct size in heart issue was detected by TTC staining, and cardiac functions were calculated according to echocardiographic evaluation. Cell viability in cardiomyocytes was investigated by Cell Counting Kit-8 (CCK-8) and lactate dehydrogenase (LDH) release assays. Western blot was used to detect autophagy-related proteins including Beclin-1, LC3, p62, adenosine 5\u2032-monophosphate (AMP)-activated protein kinase (AMPK)-mammalian target of rapamycin rabbit (mTOR)-p70 ribosomal protein S6 kinase (p70S6K) signaling-related proteins including AMPK, mTOR, p70S6K, and their phosphorylation formation. Rapamycin was used for the induction of autophagy. Cleaved caspase-3 and Bax were detected for analyzing apoptosis. TEM was used for the detection of autophagosomes. We found that CB2R deletion (CB2R KO) largely deteriorated the severity of MI and the cardiac function as well as cell viability of cardiomyocytes. Knocking out CB2R decreased the level of autophagy in heart issues from MI mice as well as cardiomyocytes under oxygen-glucose deprivation (OGD). Furthermore, CB2R dysfunction significantly attenuated the cardiac protective effects of rapamycin both in vivo and in vitro. Finally, we found that CB2R-mediated autophagy was induced by AMPK-mTOR-p70S6K signaling pathway. Our current study demonstrated for the first time that CB2R deletion led to a detrimental effect of MI through the dysfunction of AMPK-mTOR-p70S6K signaling pathway, which might provide a novel insight in the treatment of MI.<\/jats:p>","DOI":"10.1042\/bsr20180650","type":"journal-article","created":{"date-parts":[[2019,3,28]],"date-time":"2019-03-28T15:55:12Z","timestamp":1553788512000},"update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Cannabinoid receptor 2 deletion deteriorates myocardial infarction through the down-regulation of AMPK-mTOR-p70S6K signaling-mediated autophagy"],"prefix":"10.1042","volume":"39","author":[{"given":"Yao","family":"Hu","sequence":"first","affiliation":[{"name":"Cardiovascular Medicine Department, Jiangxi Provincial People\u2019s Hospital, 152 Aiguo Road, Nanchang, Jiangxi, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yu","family":"Tao","sequence":"additional","affiliation":[{"name":"Cardiovascular Medicine Department, Jiangxi Provincial People\u2019s Hospital, 152 Aiguo Road, Nanchang, Jiangxi, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5301-042X","authenticated-orcid":false,"given":"Jing","family":"Hu","sequence":"additional","affiliation":[{"name":"Cardiovascular Medicine Department, The First Hospital Of Nanchang, 128 Xiangshan North Road, Nanchang, Jiangxi, China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"288","published-online":{"date-parts":[[2019,4,26]]},"reference":[{"key":"2021111619252858800_B1","doi-asserted-by":"publisher","first-page":"743","DOI":"10.1016\/S0140-6736(15)60692-4","article-title":"Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013","volume":"386","author":"Global Burden of Disease Study C","year":"2015","journal-title":"Lancet"},{"key":"2021111619252858800_B2","doi-asserted-by":"publisher","first-page":"77","DOI":"10.1038\/nrcardio.2009.228","article-title":"Monocytes in atherosclerosis: subsets and functions","volume":"7","author":"Woollard","year":"2010","journal-title":"Nat. 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