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We propose that cancer\u2010associated lymphedema arises from destabilized receptor crosstalk within integrated lymphatic signaling units rather than solely from anatomical insufficiency. Lymphatic vessels function as multicellular signal\u2010processing systems in which receptor activity is context dependent and continuously modulated by ligand availability, tissue stiffness, inflammatory tone, and metabolic state. Under therapeutic stress, receptor systems that are secondary under homeostatic conditions, including mechanosensitive ion channels, purinergic receptors, and stress\u2010responsive G protein\u2013coupled receptors, can exert disproportionate influence over endothelial transcription, barrier function, contractile coordination, and immune\u2013vascular feedback loops. Sustained activation of these networks may reinforce inflammatory and remodeling programs, providing a mechanistic explanation for delayed onset, nonlinear progression, and interindividual variability. This signaling\u2010centered framework positions lymphatic failure after cancer therapy as a disorder of network integration and identifies stress\u2010responsive receptor systems as tractable points for early intervention.<\/jats:p>","DOI":"10.1096\/fj.202600992r","type":"journal-article","created":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T09:58:28Z","timestamp":1775642308000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Hidden Receptor Crosstalk Governs Lymphatic Failure After Cancer Therapy"],"prefix":"10.1096","volume":"40","author":[{"given":"Jim","family":"Angeles","sequence":"first","affiliation":[{"name":"Department of Physiology and Cell Biology, College of Medicine University of Arkansas for Medical Sciences  Little Rock Arkansas USA"},{"name":"Fullbright College of Arts and Sciences University of Arkansas at Fayetteville  Fayetteville Arkansas 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