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000283156 1001_ $$0P:(DE-He78)df29352b13734f9202e3b900aeef7754$$aTaylor, Jacqueline$$b0$$eFirst author$$udkfz
000283156 245__ $$aEndothelial Notch1 signaling in white adipose tissue promotes cancer cachexia.
000283156 260__ $$aLondon$$bNature Research$$c2023
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000283156 500__ $$a#EA:A270#LA:A270# / 2023 Nov;4(11):1544-1560
000283156 520__ $$aCachexia is a major cause of morbidity and mortality in individuals with cancer and is characterized by weight loss due to adipose and muscle tissue wasting. Hallmarks of white adipose tissue (WAT) remodeling, which often precedes weight loss, are impaired lipid storage, inflammation and eventually fibrosis. Tissue wasting occurs in response to tumor-secreted factors. Considering that the continuous endothelium in WAT is the first line of contact with circulating factors, we postulated whether the endothelium itself may orchestrate tissue remodeling. Here, we show using human and mouse cancer models that during precachexia, tumors overactivate Notch1 signaling in distant WAT endothelium. Sustained endothelial Notch1 signaling induces a WAT wasting phenotype in male mice through excessive retinoic acid production. Pharmacological blockade of retinoic acid signaling was sufficient to inhibit WAT wasting in a mouse cancer cachexia model. This demonstrates that cancer manipulates the endothelium at distant sites to mediate WAT wasting by altering angiocrine signals.
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000283156 7001_ $$0P:(DE-He78)97ea82956e69f88f7997e8db1a40f411$$aUhl, Leonie$$b1
000283156 7001_ $$0P:(DE-He78)68d90eb013f51c689f9ebea83a920858$$aMoll, Iris$$b2
000283156 7001_ $$0P:(DE-HGF)0$$aHasan, Sana Safatul$$b3
000283156 7001_ $$0P:(DE-He78)b27922c32bcdf07ca4d5f13ecdcfd100$$aWiedmann, Lena$$b4$$udkfz
000283156 7001_ $$aMorgenstern, Jakob$$b5
000283156 7001_ $$00000-0003-0384-325X$$aGiaimo, Benedetto Daniele$$b6
000283156 7001_ $$aFriedrich, Tobias$$b7
000283156 7001_ $$00000-0002-5761-632X$$aAlsina-Sanchis, Elisenda$$b8
000283156 7001_ $$0P:(DE-He78)95d56cbcb8b1bb5783526d136049e3df$$aDe Angelis Rigotti, Francesca$$b9
000283156 7001_ $$0P:(DE-He78)3d2b0a3563ccf6bc6ee65cf2976efe5f$$aMülfarth, Ronja$$b10
000283156 7001_ $$aKaltenbach, Sarah$$b11
000283156 7001_ $$0P:(DE-He78)b8bf46bc00efd8f5f0a915f983eb8b3d$$aSchenk, Darius$$b12
000283156 7001_ $$aNickel, Felix$$b13
000283156 7001_ $$aFleming, Thomas$$b14
000283156 7001_ $$00000-0001-6776-6957$$aSprinzak, David$$b15
000283156 7001_ $$aMogler, Carolin$$b16
000283156 7001_ $$aKorff, Thomas$$b17
000283156 7001_ $$aBilleter, Adrian T$$b18
000283156 7001_ $$aMüller-Stich, Beat P$$b19
000283156 7001_ $$aBerriel Diaz, Mauricio$$b20
000283156 7001_ $$00000-0003-4325-5452$$aBorggrefe, Tilman$$b21
000283156 7001_ $$aHerzig, Stephan$$b22
000283156 7001_ $$00000-0003-3926-1534$$aRohm, Maria$$b23
000283156 7001_ $$00000-0001-9547-5508$$aRodriguez-Vita, Juan$$b24
000283156 7001_ $$0P:(DE-He78)039283a5d51058ec79156d0ef67132da$$aFischer, Andreas$$b25$$eLast author$$udkfz
000283156 773__ $$0PERI:(DE-600)3005299-3$$a10.1038/s43018-023-00622-y$$n11$$p1544-1560$$tNature cancer$$v4$$x2662-1347$$y2023
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