Relationship of aging and cardiac IL-10

Victoria Dotson, Katherine Horak, Cory Alwardt, Douglas F Larson

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

Current therapies for the treatment of myocardial infarction and heart failure include medical, surgical, mechanical assist, and transplantation. These therapies have been based on the dogma that ventricular myocytes themselves are terminally differentiated and, therefore, cannot regenerate. This concept has been recently challenged with stem cell therapy. A potential problem is the ability of cardiac tissue to mobilize, recruit, and transdifferentiate adult stem cells from other tissues. We believe that there is a unique failure of the damaged myocardium to provide the appropriate molecular signals for stem cells engraftment related to age. Our hypothesis is that the overexpression of IL-10 in the aged population reduces cardiac cellular proliferation subsequent to myocardial injury. This hypothesis is supported by aging models, where elevated levels of IL-10 are associated with reduced healing response to noncardiac tissue injury. We demonstrated an increased cardiac gene expression of IL-10 that may be associated with a reduced proliferative response in the border regions of the infarcted myocardium that are proportional with age. In conclusion, myocardial infarction and heart failure has presented a significant challenge for the clinician to provide reparative therapies. The use of therapeutics to modulate IL-10 and, thereby, optimizing regenerative processes in the injured myocardium may provide a unique means for the cardiac patient.

Original languageEnglish (US)
Pages (from-to)197-201
Number of pages5
JournalJournal of Extra-Corporeal Technology
Volume36
Issue number2
Publication statusPublished - Jun 2004

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Keywords

  • Aging
  • IL-10, stem cells
  • Myocardial regeneration

ASJC Scopus subject areas

  • Medicine (miscellaneous)

Cite this

Dotson, V., Horak, K., Alwardt, C., & Larson, D. F. (2004). Relationship of aging and cardiac IL-10. Journal of Extra-Corporeal Technology, 36(2), 197-201.