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Moreover,\n                      <jats:italic>in vitro<\/jats:italic>\n                      studies suggest an interference of cannabinoid\u2010signalling with cardiomyocyte contractility and hypertrophy. We aimed at revealing a functional contribution of the cannabinoid\u2010sensitive receptor GPR55 to cardiomyocyte homeostasis and neurohumorally induced hypertrophy\n                      <jats:italic>in vivo<\/jats:italic>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Gpr55<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>\u2212\/\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      and wild\u2010type (WT) mice were characterized after 28\u2010day angiotensin II (AngII; 1\u00b7\u03bcg\u00b7kg\n                      <jats:sup>\u22121<\/jats:sup>\n                      \u00a0min\n                      <jats:sup>\u22121<\/jats:sup>\n                      ) or vehicle infusion. In isolated adult\n                      <jats:italic>Gpr55<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>\u2212\/\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      and WT cardiomyocytes, mitochondrial function was assessed under na\u00efve conditions, while cytosolic Ca\n                      <jats:sup>2+<\/jats:sup>\n                      handling was additionally determined following application of the selective GPR55 antagonist CID16020046.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Gpr55<\/jats:italic>\n                      deficiency did not affect angiotensin II (AngII) mediated hypertrophic growth, yet, especially in females, it alleviated maladaptive pro\u2010hypertrophic and \u2010inflammatory gene expression and improved inotropy and adrenergic responsiveness compared to WT. In\u2010depth analyses implied increased cytosolic Ca\n                      <jats:sup>2+<\/jats:sup>\n                      concentrations and transient amplitudes, and accelerated sarcomere contraction kinetics in\n                      <jats:italic>Gpr55<\/jats:italic>\n                      <jats:sup>\n                        <jats:italic>\u2212\/\u2212<\/jats:italic>\n                      <\/jats:sup>\n                      myocytes, which could be mimicked by GPR55 blockade with CID16020046 in female WT cells. Moreover,\n                      <jats:italic>Gpr55<\/jats:italic>\n                      deficiency up\u2010regulated factors involved in glucose and fatty acid transport independent of the AngII challenge, accelerated basal mitochondrial respiration and reduced basal protein kinase (PK) A, G and C activity and phospholemman (PLM) phosphorylation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Implications<\/jats:title>\n                    <jats:p>Our study suggests GPR55 as crucial regulator of cardiomyocyte hypertrophy and homeostasis presumably by regulating PKC\/PKA\u2010PLM and PKG signalling, and identifies the receptor as potential target to counteract maladaptation, adrenergic desensitization and metabolic shifts as unfavourable features of the hypertrophied heart in females.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.17350","type":"journal-article","created":{"date-parts":[[2024,10,21]],"date-time":"2024-10-21T00:20:09Z","timestamp":1729470009000},"page":"670-691","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["<i>Gpr55<\/i>\n                    deficiency crucially alters cardiomyocyte homeostasis and counteracts angiotensin II induced maladaption in female mice"],"prefix":"10.1111","volume":"182","author":[{"given":"Brigitte","family":"Schopohl","sequence":"first","affiliation":[{"name":"Institute for Cardiovascular Prevention (IPEK) Ludwig\u2010Maximilians\u2010Universit\u00e4t (LMU) Munich  Munich Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Kohlhaas","sequence":"additional","affiliation":[{"name":"Comprehensive Heart Failure Center University Clinic W\u00fcrzburg  W\u00fcrzburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander G.","family":"Nickel","sequence":"additional","affiliation":[{"name":"Comprehensive Heart Failure Center University Clinic W\u00fcrzburg  W\u00fcrzburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna\u2010Florentine","family":"Schiuma","sequence":"additional","affiliation":[{"name":"Comprehensive Heart Failure Center University Clinic W\u00fcrzburg  W\u00fcrzburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanne L.","family":"Maas","sequence":"additional","affiliation":[{"name":"Institute for Molecular Cardiovascular Research (IMCAR) RWTH Aachen University  Aachen Germany"},{"name":"Interdisciplinary Center for Clinical Research (IZKF) RWTH Aachen University  Aachen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emiel P. 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