Document Type
Article
Language
eng
Format of Original
5 p.
Publication Date
2-28-2011
Publisher
Elsevier
Source Publication
Life Sciences
Source ISSN
0024-3205
Original Item ID
doi: 10.1016/j.lfs.2010.12.010
Abstract
Aims
Fatigue is a common occurrence in cancer patients regardless of tumor type or anti-tumor therapies and is an especially problematic symptom in persons with incurable tumor disease. In rodents, tumor-induced fatigue is associated with a progressive loss of skeletal muscle mass and increased expression of biomarkers of muscle protein degradation. The purpose of the present study was to determine if muscle wasting and expression of biomarkers of muscle protein degradation occur in the hearts of tumor-bearing mice, and if these effects of tumor growth are associated with changes in cardiac function.
Main methods
The colon26 adenocarcinoma cell line was implanted into female CD2F1 mice and skeletal muscle wasting, in vivo heart function, in vitro cardiomyocyte function, and biomarkers of muscle protein degradation were determined.
Key findings
Expression of biomarkers of protein degradation were increased in both the gastrocnemius and heart muscle of tumor-bearing mice and caused systolic dysfunction in vivo. Cardiomyocyte function was significantly depressed during both cellular contraction and relaxation.
Significance
These results suggest that heart muscle is directly affected by tumor growth, with myocardial function more severely compromised at the cellular level than what is observed using echocardiography.
Recommended Citation
Xu, Hui; Crawford, Danielle; Hutchinson, Kirk R.; Youtz, Dane J.; Lucchesi, Pamela A.; Velten, Markus; McCarthy, Donna O.; and Wold, Loren E., "Myocardial Dysfunction in an Animal Model of Cancer Cachexia" (2011). College of Nursing Faculty Research and Publications. 188.
https://epublications.marquette.edu/nursing_fac/188
Comments
Accepted version. Life Sciences, Vol. 88, No. 9-10 (February 28, 2011): 406-410. DOI. © 2011 Elsevier. Used with permission.
Donna McCarthy was affiliated with The Ohio State University at the time of publication.