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Endothelial cells are activated after I\/R, which may drive the inflammatory response by releasing ATP through pannexin1 (Panx1) channels. Here, we investigated the role of Panx1 in cardiac I\/R.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Panx1 was found in cardiac endothelial cells, neutrophils, and cardiomyocytes. After in vivo I\/R, serum Troponin-I, and infarct size were less pronounced in Panx1\u2212\/\u2212 mice, but leukocyte infiltration in the infarct area was similar between Panx1\u2212\/\u2212 and wild-type mice. Serum Troponin-I and infarct size were not different between mice with neutrophil-specific deletion of Panx1 and Panx1fl\/fl mice, suggesting that cardioprotection by Panx1 deletion rather involved cardiomyocytes than the inflammatory response. Physiological cardiac function in wild-type and Panx1\u2212\/\u2212 hearts was similar. The time to onset of contracture and time to maximal contracture were delayed in Panx1\u2212\/\u2212 hearts, suggesting reduced sensitivity of these hearts to ischaemic injury. Moreover, Panx1\u2212\/\u2212 hearts showed better recovery of left ventricle developed pressure, cardiac contractility, and relaxation after I\/R. Ischaemic preconditioning failed to confer further protection in Panx1\u2212\/\u2212 hearts. Panx1 was found in subsarcolemmal mitochondria (SSM). SSM in WT or Panx1\u2212\/\u2212 hearts showed no differences in morphology. The function of the mitochondrial permeability transition pore and production of reactive oxygen species in SSM was not affected, but mitochondrial respiration was reduced in Panx1\u2212\/\u2212 SSM. Finally, Panx1\u2212\/\u2212 cardiomyocytes had a decreased mitochondrial membrane potential and an increased mitochondrial ATP content.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Panx1\u2212\/\u2212 mice display decreased sensitivity to cardiac I\/R injury, resulting in smaller infarcts and improved recovery of left ventricular function. This cardioprotective effect of Panx1 deletion seems to involve cardiac mitochondria rather than a reduced inflammatory response. Thus, Panx1 may represent a new target for controlling cardiac reperfusion damage.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvad120","type":"journal-article","created":{"date-parts":[[2023,7,28]],"date-time":"2023-07-28T16:35:54Z","timestamp":1690562154000},"page":"2342-2354","source":"Crossref","is-referenced-by-count":27,"title":["Mitochondrial pannexin1 controls cardiac sensitivity to ischaemia\/reperfusion injury"],"prefix":"10.1093","volume":"119","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3540-4737","authenticated-orcid":false,"given":"Olga M","family":"Rusiecka","sequence":"first","affiliation":[{"name":"Department of Pathology and Immunology, Faculty of Medicine, University of Geneva , Rue Michel-Servet 1, CH-1211 Geneva , Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0405-5397","authenticated-orcid":false,"given":"Filippo","family":"Molica","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Faculty of Medicine, University of Geneva , Rue Michel-Servet 1, CH-1211 Geneva , Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9718-5421","authenticated-orcid":false,"given":"Morten S","family":"Nielsen","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen , Copenhagen , Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2189-3402","authenticated-orcid":false,"given":"Axel","family":"Tollance","sequence":"additional","affiliation":[{"name":"Department of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva , Geneva , Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1538-3553","authenticated-orcid":false,"given":"Sandrine","family":"Morel","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Faculty of Medicine, University of Geneva , Rue Michel-Servet 1, CH-1211 Geneva , Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7135-0874","authenticated-orcid":false,"given":"Maud","family":"Frieden","sequence":"additional","affiliation":[{"name":"Department of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva , Geneva , Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8104-2090","authenticated-orcid":false,"given":"Marc","family":"Chanson","sequence":"additional","affiliation":[{"name":"Department of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva , Geneva , Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kerstin","family":"Boengler","sequence":"additional","affiliation":[{"name":"Institute of Physiology, Justus-Liebig University , Giessen , Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0015-0044","authenticated-orcid":false,"given":"Brenda R","family":"Kwak","sequence":"additional","affiliation":[{"name":"Department of Pathology and Immunology, Faculty of Medicine, University of Geneva , Rue Michel-Servet 1, CH-1211 Geneva , Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2023,8,9]]},"reference":[{"key":"2023102421133529300_cvad120-B1","doi-asserted-by":"crossref","first-page":"716","DOI":"10.1093\/eurheartj\/ehab892","article-title":"European Society of cardiology: cardiovascular disease statistics 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