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For example, in the field of myocardial infarction (MI), new aspects of autophagy and the importance of eosinophils were described. Novel approaches, such as a glycocalyx mimetic, were used to improve cardiac recovery following MI. The strategy of 3D bio-printing was shown to allow the fabrication of a chambered cardiac organoid. The benefit of combining tissue engineering with paracrine therapy to heal injured myocardium is discussed. We highlight the importance of cell-to-cell communication, in particular, the relevance of extracellular vesicles, such as exosomes, which transport proteins, lipids, non-coding RNAs, and mRNAs and actively contribute to angiogenesis and myocardial regeneration. In this rapidly growing field, new strategies were developed to stimulate the release of reparative exosomes in ischaemic myocardium. Single-cell sequencing technology is causing a revolution in the study of transcriptional expression at cellular resolution, revealing unanticipated heterogeneity within cardiomyocytes, pericytes and fibroblasts, and revealing a unique subpopulation of cardiac fibroblasts. Several studies demonstrated that exosome- and non-coding RNA-mediated approaches can enhance human induced pluripotent stem cell (iPSC) viability and differentiation into mature cardiomyocytes. Important details of the mitochondrial Ca2+ uniporter and its relevance were elucidated. Novel aspects of cancer therapeutic-induced cardiotoxicity were described, such as the novel circular RNA circITCH, which may lead to novel treatments. Finally, we provide some insights into the effects of SARS-CoV-2 on the heart.<\/jats:p>","DOI":"10.1093\/cvr\/cvab200","type":"journal-article","created":{"date-parts":[[2021,6,9]],"date-time":"2021-06-09T19:23:20Z","timestamp":1623266600000},"page":"2161-2174","source":"Crossref","is-referenced-by-count":52,"title":["Progress in cardiac research: from rebooting cardiac regeneration to a complete cell atlas of the heart"],"prefix":"10.1093","volume":"117","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5182-4980","authenticated-orcid":false,"given":"Sean M","family":"Davidson","sequence":"first","affiliation":[{"name":"The Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London WC1E 6HX, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1921-954X","authenticated-orcid":false,"given":"Teresa","family":"Padr\u00f3","sequence":"additional","affiliation":[{"name":"Cardiovascular Program ICCC, Institut de Recerca de l'Hospital Santa Creu i Sant Pau-IIB Sant Pau, Barcelona, Spain"},{"name":"CIBER Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III (ISCIII), Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sveva","family":"Bollini","sequence":"additional","affiliation":[{"name":"Department of Experimental Medicine (DIMES), University of Genova, Genova, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gemma","family":"Vilahur","sequence":"additional","affiliation":[{"name":"Cardiovascular Program ICCC, Institut de Recerca de l'Hospital Santa Creu i Sant Pau-IIB Sant Pau, Barcelona, Spain"},{"name":"CIBER Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III (ISCIII), Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2836-2241","authenticated-orcid":false,"given":"Dirk J","family":"Duncker","sequence":"additional","affiliation":[{"name":"Division of Experimental Cardiology, Department of Cardiology, Thoraxcenter, Erasmus University Medical Center, Rotterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul C","family":"Evans","sequence":"additional","affiliation":[{"name":"Department of Infection, Immunity and Cardiovascular Disease and Insigneo Institute, University of Sheffield, Sheffield, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomasz","family":"Guzik","sequence":"additional","affiliation":[{"name":"British Heart Foundation Centre for Cardiovascular Research, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK"},{"name":"Department of Medicine, Jagiellonian University, Collegium Medicum, Krakow, Poland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8379-7814","authenticated-orcid":false,"given":"Imo E","family":"Hoefer","sequence":"additional","affiliation":[{"name":"Central Diagnostic Laboratory, University Medical Center Utrecht, Utrecht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2417-9880","authenticated-orcid":false,"given":"Johannes","family":"Waltenberger","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Medical Faculty, University of Muenster, Muenster, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1282-9276","authenticated-orcid":false,"given":"Johann","family":"Wojta","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4610-8714","authenticated-orcid":false,"given":"Christian","family":"Weber","sequence":"additional","affiliation":[{"name":"Institute for Cardiovascular Prevention (IPEK), LMU Munich, DZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, and Munich Cluster for Systems Neurology (SyNergy), Munich, Germany"},{"name":"Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2021,6,11]]},"reference":[{"key":"2021083012410474500_cvab200-B1","doi-asserted-by":"crossref","first-page":"645","DOI":"10.1093\/cvr\/cvz152","article-title":"TXNIP\/Redd1 signalling and excessive autophagy: a novel mechanism of myocardial ischaemia\/reperfusion injury in 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