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We investigated the role of GPR55 in cardiac physiology and post-MI inflammation and remodelling. Global GPR55\u2212\/\u2212 and wildtype (WT) mice were basally characterized or assigned to 1, 3 or 28\u00a0days permanent MI and subsequently analysed via pro-inflammatory and pro-hypertrophic parameters. GPR55\u2212\/\u2212 deficiency was basally associated with bradycardia, increased diastolic LV volume and sarcomere length and a subtle inflammatory phenotype. While infarct size and myeloid cell infiltration were unaffected by GPR55 depletion, acute cardiac chemokine production was prolonged post-MI. Concurrently, GPR55\u2212\/\u2212 hearts exhibited a premature expansion of pro-reparative and phagocytic macrophages paralleled by early up-regulation of extracellular matrix (ECM) factors 3\u00a0days post-MI, which could be mimicked by sole haematopoietic GPR55 depletion. Moreover, global GPR55 deficiency mitigated MI-induced foetal gene re-programming and cardiomyocyte hypertrophy, culminating in aggravated LV dilatation and infarct expansion. GPR55 regulates cardiac homeostasis and ischaemia responses by maintaining adequate LV filling and modulating three crucial processes post-MI: wound healing kinetics, cardiomyocyte hypertrophy and maladaptive remodelling.<\/jats:p>","DOI":"10.1038\/s41598-021-93755-y","type":"journal-article","created":{"date-parts":[[2021,7,13]],"date-time":"2021-07-13T06:24:02Z","timestamp":1626157442000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling"],"prefix":"10.1038","volume":"11","author":[{"given":"Sarah-Lena","family":"Puhl","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Hilby","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Kohlhaas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linus M.","family":"Keidel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yvonne","family":"Jansen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Hristov","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jakob","family":"Schindler","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christoph","family":"Maack","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabine","family":"Steffens","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,7,13]]},"reference":[{"key":"93755_CR1","doi-asserted-by":"publisher","first-page":"414","DOI":"10.1016\/j.cardiores.2003.12.023","volume":"61","author":"F Eefting","year":"2004","unstructured":"Eefting, F. et al. 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