ArticleNature cancer2023
Endothelial Notch1 signaling in white adipose tissue promotes cancer cachexia.
Article in Nature cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 24 citations in OpenAlex.
- Unveiling the mechanism of Baoyuan Jiedu Decoction in cancer cachexia-induced lipolysis through network pharmacology and bioinformatics.Journal of traditional and complementary medicine · 2026Article
- LRRFIP1 Inhibits White Adipocyte Differentiation by Suppressing the E2F6/C/EBPα Axis.Diabetes & metabolism journal · 2026Article
- Otopetrin 1 protects against adipose tissue wasting during cancer cachexia progression.iScience · 2026Article
- Review
- [18 F]FDG PET unveils a cachexia-specific multiorgan metabolic phenotype and identifies patients with poor prognosis in locally advanced rectal cancer.European journal of nuclear medicine and molecular imaging · 2026Article
- Impaired Adipose Anabolism in Pancreatic Cancer Cachexia Is Reversed by HuR Inhibition.Journal of cachexia, sarcopenia and muscle · 2026Article
- Targeting a super-enhancer induced aldehyde dehydrogenase metabolic loop mitigates CDK4/6 inhibitor resistance in estrogen receptor-positive cancers.Nature communications · 2026Article
- CircAMOTL1 promotes adipose lipolysis and browning in cancer cachexia through miR-211-5p-mediated TET2 activation.The Journal of biological chemistry · 2026Article
- Defining the vascular niche of human adipose tissue across metabolic states.Nature metabolism · 2026Article
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- The FGL1-LAG-3 axis attenuates melanoma-induced cachexia in mice.Cancer & metabolism · 2026Article
- Cancer-Associated Cachexia in the Era of Obesity.International journal of molecular sciences · 2025Review
- Defining the vascular niche of human adipose tissue across metabolic states.bioRxiv : the preprint server for biology · 2025Article
- The RNA-binding protein HuR impairs adipose tissue anabolism in pancreatic cancer cachexia.bioRxiv : the preprint server for biology · 2025Article
- Cancer-Associated Cachexia: Bridging Clinical Findings with Mechanistic Insights in Human Studies.Cancer discovery · 2025Review
- Skeletal muscle endothelial dysfunction through the activin A-PGC1α axis drives progression of cancer cachexia.Nature cancer · 2025Article
- NOTCH Signaling Networks in Perivascular Adipose Tissue.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Cancer cachexia: multilevel metabolic dysfunction.Nature metabolism · 2024Review
- Targeting the tumour vasculature: from vessel destruction to promotion.Nature reviews. Cancer · 2024Review
- Review
Corrections and comments
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Authors and funding
26 authors at 6 institutions in 3 countries.
Funding
Abstract
Cachexia 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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.