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Despite enormous advances in deciphering the molecular mechanisms underlying heart failure progression, the cell-type specific adaptations and especially intercellular signaling remain poorly understood. Cardiac fibroblasts express high levels of cardiogenic transcription factors such as GATA-4 and GATA-6, but their role in fibroblasts during stress is not known. Here, we show that fibroblast GATA-4 and GATA-6 promote adaptive remodeling in pressure overload induced cardiac hypertrophy. Using a mouse model with specific single or double deletion of\n                    <jats:italic>Gata4<\/jats:italic>\n                    and\n                    <jats:italic>Gata6<\/jats:italic>\n                    in stress activated fibroblasts, we found a reduced myocardial capillarization in mice with\n                    <jats:italic>Gata4\/6<\/jats:italic>\n                    double deletion following pressure overload, while single deletion of\n                    <jats:italic>Gata4<\/jats:italic>\n                    or\n                    <jats:italic>Gata6<\/jats:italic>\n                    had no effect. Importantly, we confirmed the reduced angiogenic response using an in vitro co-culture system with\n                    <jats:italic>Gata4\/6<\/jats:italic>\n                    deleted cardiac fibroblasts and endothelial cells. A comprehensive RNA-sequencing analysis revealed an upregulation of anti-angiogenic genes upon\n                    <jats:italic>Gata4\/6<\/jats:italic>\n                    deletion in fibroblasts, and siRNA mediated downregulation of these genes restored endothelial cell growth. In conclusion, we identified a novel role for the cardiogenic transcription factors GATA-4 and GATA-6 in heart fibroblasts, where both proteins act in concert to promote myocardial capillarization and heart function by directing intercellular crosstalk.\n                  <\/jats:p>","DOI":"10.1007\/s00395-021-00862-y","type":"journal-article","created":{"date-parts":[[2021,4,19]],"date-time":"2021-04-19T13:03:34Z","timestamp":1618837414000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":53,"title":["Fibroblast GATA-4 and GATA-6 promote myocardial adaptation to pressure overload by enhancing cardiac angiogenesis"],"prefix":"10.1007","volume":"116","author":[{"given":"Gesine M.","family":"Dittrich","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natali","family":"Froese","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xue","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannah","family":"Kroeger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Honghui","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Malgorzata","family":"Szaroszyk","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mona","family":"Malek-Mohammadi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julio","family":"Cordero","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Merve","family":"Keles","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mortimer","family":"Korf-Klingebiel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai C.","family":"Wollert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Geffers","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuel","family":"Mayr","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon J.","family":"Conway","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gergana","family":"Dobreva","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johann","family":"Bauersachs","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1541-3030","authenticated-orcid":false,"given":"Joerg","family":"Heineke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,4,19]]},"reference":[{"key":"862_CR1","doi-asserted-by":"publisher","first-page":"789","DOI":"10.1161\/CIRCULATIONAHA.111.056952","volume":"125","author":"J Barallobre-Barreiro","year":"2012","unstructured":"Barallobre-Barreiro J, Didangelos A, Schoendube FA, Drozdov I, Yin X, Fernandez-Caggiano M, Willeit P, Puntmann VO, Aldama-Lopez G, Shah AM, Domenech N, Mayr M (2012) Proteomics analysis of cardiac extracellular matrix remodeling in a porcine model of ischemia\/reperfusion injury. 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