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dc.contributor.authorMeçe, Odeta
dc.contributor.authorHoubaert, Diede
dc.contributor.authorSassano, Maria-Livia
dc.contributor.authorDurré, Tania
dc.contributor.authorMaes, Hannelore
dc.contributor.authorSchaaf, Marco
dc.contributor.authorMore, Sanket
dc.contributor.authorGanne, Maarten
dc.contributor.authorGarcía-Caballero, Melissa
dc.contributor.authorBorn, Mila
dc.contributor.authorVerhoeven, Jelle
dc.contributor.authorAgrawal, Madhur
dc.contributor.authorJacobs, Kathryn
dc.contributor.authorBergers, Gabriele
dc.contributor.authorBlacher, Silvia
dc.contributor.authorGhesquière, Bart
dc.contributor.authorDewerchin, Mieke
dc.contributor.authorSwinnen, Johan V.
dc.contributor.authorVinckier, Stefan
dc.contributor.authorSoengas, María S.
dc.contributor.authorCarmeliet, Peter
dc.contributor.authorNoël, Agnès
dc.contributor.authorAgostinis, Patrizia
dc.date.accessioned2023-06-28T09:57:48Z
dc.date.available2023-06-28T09:57:48Z
dc.date.created2023-06-28
dc.date.issued2022-05-19
dc.identifier.citationMeçe, O., Houbaert, D., Sassano, ML. et al. Lipid droplet degradation by autophagy connects mitochondria metabolism to Prox1-driven expression of lymphatic genes and lymphangiogenesis. Nat Commun 13, 2760 (2022). https://doi.org/10.1038/s41467-022-30490-6
dc.identifier.urihttps://hdl.handle.net/10630/27105
dc.description.abstractAutophagy has vasculoprotective roles, but whether and how it regulates lymphatic endothelial cells (LEC) homeostasis and lymphangiogenesis is unknown. Here, we show that genetic deficiency of autophagy in LEC impairs responses to VEGF-C and injury-driven corneal lymphangiogenesis. Autophagy loss in LEC compromises the expression of main effectors of LEC identity, like VEGFR3, affects mitochondrial dynamics and causes an accumulation of lipid droplets (LDs) in vitro and in vivo. When lipophagy is impaired, mitochondrial ATP production, fatty acid oxidation, acetyl-CoA/CoA ratio and expression of lymphangiogenic PROX1 target genes are dwindled. Enforcing mitochondria fusion by silencing dynamin-related-protein 1 (DRP1) in autophagy-deficient LEC fails to restore LDs turnover and lymphatic gene expression, whereas supplementing the fatty acid precursor acetate rescues VEGFR3 levels and signaling, and lymphangiogenesis in LEC-Atg5−/− mice. Our findings reveal that lipophagy in LEC by supporting FAO, preserves a mitochondrial-PROX1 gene expression circuit that safeguards LEC responsiveness to lymphangiogenic mediators and lymphangiogenesis.es_ES
dc.language.isoenges_ES
dc.publisherSpringerNature
dc.rightsinfo:eu-repo/semantics/openAccesses_ES
dc.subjectCélulas - Metabolismo
dc.subject.otherLympahticses_ES
dc.subject.otherProx1
dc.subject.otherLipid droplets
dc.subject.otherAutophagy
dc.titleLipid droplet degradation by autophagy connects mitochondria metabolism to Prox1-driven expression of lymphatic genes and lymphangiogenesis.es_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.identifier.doi10.1038/s41467-022-30490-6
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion


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