Journal
THYMOSINS IN HEALTH AND DISEASE I
Volume 1269, Issue -, Pages 92-101Publisher
BLACKWELL SCIENCE PUBL
DOI: 10.1111/j.1749-6632.2012.06708.x
Keywords
thymosin beta 4; EPDCs; epicardium; Wt1; myocardial regeneration; de novo cardiomyocytes
Categories
Funding
- British Heart Foundation
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL094683] Funding Source: NIH RePORTER
- British Heart Foundation [RG/08/015/26411, FS/08/004/23625] Funding Source: researchfish
- Engineering and Physical Sciences Research Council [EP/I014667/1] Funding Source: researchfish
- Medical Research Council [G0700933] Funding Source: researchfish
- EPSRC [EP/I014667/1] Funding Source: UKRI
- MRC [G0700933] Funding Source: UKRI
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Efficient cardiac regeneration postinfarction (MI) requires the replacement of lost cardiomyocytes, formation of new coronary vessels and appropriate modulation of the inflammatory response. However, insight into how to stimulate repair of the human heart is currently limited. Using the embryonic paradigm of regeneration, we demonstrated that the actin-binding peptide thymosin beta 4 (T beta 4), required for epicardium-derived coronary vasculogenesis, can recapitulate its embryonic role and activate quiescent adult epicardial cells (EPDCs). Once stimulated, EPDCs facilitate neovascularization of the ischemic adult heart and, moreover, contribute bona fide cardiomyocytes. EPDC-derived cardiomyocytes structurally and functionally integrate with resident muscle to regenerate functional myocardium, limiting pathological remodeling, and effecting an improvement in cardiac function. Alongside pro-survival and anti-inflammatory properties, these regenerative roles, via EPDCs, markedly expand the range of therapeutic benefits of T beta 4 to sustain and repair the myocardium after ischemic damage.
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