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Activin receptor type 2B (ACVR2B) signalling is known to cause SKM wasting, and its inhibition restores SKM mass and prolongs survival in cancer. Using a recently generated mouse model, here we tested whether ACVR2B blockade could preserve multiple organs, including skeletal and cardiac muscle, in the presence of metastatic CRC.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>NSG male mice (8\u00a0weeks old) were injected intrasplenically with HCT116 human CRC cells (mHCT116), while sham\u2010operated animals received saline (<jats:italic>n<\/jats:italic>\u00a0=\u00a05\u201310 per group). Sham and tumour\u2010bearing mice received weekly injections of ACVR2B\/Fc, a synthetic peptide inhibitor of ACVR2B.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>mHCT116 hosts displayed losses in fat mass (\u2009\u2212\u200979%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.0001), bone mass (\u2009\u2212\u200939%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05), and SKM mass (quadriceps:\u00a0\u2212\u200922%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.001), in line with reduced muscle cross\u2010sectional area (\u2009\u2212\u200924%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.01) and plantarflexion force (\u2009\u2212\u200928%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05). Further, despite only moderately affected heart size, cardiac function was significantly impaired (ejection fraction %:\u00a0\u2212\u200916%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.0001; fractional shortening %:\u00a0\u2212\u200925%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.0001) in the mHCT116 hosts. Conversely, ACVR2B\/Fc preserved fat mass (\u2009+\u2009238%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.001), bone mass (\u2009+\u2009124%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.0001), SKM mass (quadriceps:\u00a0+\u200931%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.0001), size (cross\u2010sectional area:\u00a0+\u200943%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.0001) and plantarflexion force (\u2009+\u200928%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.05) in tumour hosts. Cardiac function was also completely preserved in tumour hosts receiving ACVR2B\/Fc (ejection fraction %:\u00a0+\u200919%, <jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00.0001), despite no effect on heart size. RNA sequencing analysis of heart muscle revealed rescue of genes related to cardiac development and contraction in tumour hosts treated with ACVR2B\/Fc.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our metastatic CRC model recapitulates the multi\u2010systemic derangements of cachexia by displaying loss of fat, bone, and SKM along with decreased muscle strength in mHCT116 hosts. Additionally, with evidence of severe cardiac dysfunction, our data support the development of cardiac cachexia in the occurrence of metastatic CRC. Notably, ACVR2B antagonism preserved adipose tissue, bone, and SKM, whereas muscle and cardiac functions were completely maintained upon treatment. Altogether, our observations implicate ACVR2B signalling in the development of multi\u2010organ perturbations in metastatic CRC and further dictate that ACVR2B represents a promising therapeutic target to preserve body composition and functionality in cancer cachexia.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcsm.12642","type":"journal-article","created":{"date-parts":[[2020,11,17]],"date-time":"2020-11-17T05:16:14Z","timestamp":1605590174000},"page":"1779-1798","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["ACVR2B antagonism as a countermeasure to multi\u2010organ perturbations in metastatic colorectal cancer cachexia"],"prefix":"10.1002","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8632-5791","authenticated-orcid":false,"given":"Joshua R.","family":"Huot","sequence":"first","affiliation":[{"name":"Department of Surgery Indiana University School of Medicine  Indianapolis IN 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