Journal
CELL METABOLISM
Volume 31, Issue 5, Pages 987-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2020.04.007
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Funding
- Associazione Italiana per la Ricerca sul Cancro (AIRC) [IG19991, IG15748, IG19928]
- European Research Council (ERC) [FP7-282280]
- European Union FP7 CIG [PCIG13GA-2013-618697]
- Ministero dell'Istruzione, dell'Universita e della Ricerca (MIUR) [FIRB RBAP11Z3YA_005, PRIN 2017BF3PXZ, PRIN 2017FS5SHL]
- University of Padua STARS Consolidator FIRMESs
- ERC [H2020-725004]
- CERCA Programme/Generalitat de Catalunya
- European Foundation for the Study of Diabetes (EFSD)/Lilly Research grant
- MINECO (Spain) - European Regional Developmental Fund (ERDF), a Way to Build Europe [SAF2017-89116R-P]
- FP7-Cofund DTI-IMPORT
- AIRC Fellowship
- Fonds Leon Fredericq (University of Liege)
- Foundation Umberto Veronesi fellowship
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While endothelial cell (EC) function is influenced by mitochondrialmetabolism, the role ofmitochondrial dynamics in angiogenesis, the formation of new blood vessels from existing vasculature, is unknown. Here we show that the inner mitochondrial membrane mitochondrial fusion protein optic atrophy 1 (OPA1) is required for angiogenesis. In response to angiogenic stimuli, OPA1 levels rapidly increase to limit nuclear factor kappa-light-chain-enhancer of activated B cell (NFkB) signaling, ultimately allowing angiogenic genes expression and angiogenesis. Endothelial Opa1 is indeed required in an NFkB-dependent pathway essential for developmental and tumor angiogenesis, impacting tumor growth and metastatization. A firstin-class small molecule-specific OPA1 inhibitor confirms that EC Opa1 can be pharmacologically targeted to curtail tumor growth. Our data identify Opa1 as a crucial component of physiological and tumor angiogenesis.
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