{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,9]],"date-time":"2026-11-09T10:17:30Z","timestamp":1794219450336,"version":"4.8.0"},"reference-count":149,"publisher":"MDPI AG","issue":"12","license":[{"start":{"date-parts":[[2022,6,15]],"date-time":"2022-06-15T00:00:00Z","timestamp":1655251200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Cancer cachexia is a syndrome of progressive weight loss and muscle wasting occurring in many advanced cancer patients. Cachexia significantly impairs quality of life and increases mortality. Cardiac atrophy and dysfunction have been observed in patients with cachexia, which may contribute to cachexia pathophysiology. However, relative to skeletal muscle, little research has been carried out to understand the mechanisms of cardiomyopathy in cachexia. Here, we review what is known clinically about the cardiac changes occurring in cachexia, followed by further discussion of underlying physiological and molecular mechanisms contributing to cachexia-induced cardiomyopathy. Impaired cardiac contractility and relaxation may be explained by a complex interplay of significant heart muscle atrophy and metabolic remodeling, including mitochondrial dysfunction. Because cardiac muscle has fundamental differences compared to skeletal muscle, understanding cardiac-specific effects of cachexia may bring light to unique therapeutic targets and ultimately improve clinical management for patients with cancer cachexia.<\/jats:p>","DOI":"10.3390\/cells11121931","type":"journal-article","created":{"date-parts":[[2022,6,15]],"date-time":"2022-06-15T22:17:01Z","timestamp":1655331421000},"page":"1931","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Cardiac Remodeling in Cancer-Induced Cachexia: Functional, Structural, and Metabolic Contributors"],"prefix":"10.3390","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5901-7515","authenticated-orcid":false,"given":"Michael P.","family":"Wiggs","sequence":"first","affiliation":[{"name":"Department of Health, Human Performance, and Recreation, Robbins College of Health and Human Sciences, Baylor University, Waco, TX 76706, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna G.","family":"Beaudry","sequence":"additional","affiliation":[{"name":"Department of Health, Human Performance, and Recreation, Robbins College of Health and Human Sciences, Baylor University, Waco, TX 76706, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5570-0376","authenticated-orcid":false,"given":"Michelle L.","family":"Law","sequence":"additional","affiliation":[{"name":"Department of Human Sciences and Design, Robbins College of Health and Human Sciences, Baylor University, Waco, TX 76706, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2022,6,15]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"22","DOI":"10.1002\/jcsm.12402","article-title":"Orphan Disease Status of Cancer Cachexia in the USA and in the European Union: A Systematic Review","volume":"10","author":"Anker","year":"2019","journal-title":"J. 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