Thymosin β4 and cardiac repair

Department of Cardiovascular and Thoracic Surgery, University of Texas, Southwestern Medical Center, Dallas, Texas, USA.
Annals of the New York Academy of Sciences (Impact Factor: 4.38). 04/2010; 1194(1):87-96. DOI: 10.1111/j.1749-6632.2010.05468.x
Source: PubMed


Hypoxic heart disease is a predominant cause of disability and death worldwide. As adult mammals are incapable of cardiac repair after infarction, the discovery of effective methods to achieve myocardial and vascular regeneration is crucial. Efforts to use stem cells to repopulate damaged tissue are currently limited by technical considerations and restricted cell potential. We discovered that the small, secreted peptide thymosin beta4 (Tbeta4) could be sufficiently used to inhibit myocardial cell death, stimulate vessel growth, and activate endogenous cardiac progenitors by reminding the adult heart on its embryonic program in vivo. The initiation of epicardial thickening accompanied by increase of myocardial and epicardial progenitors with or without infarction indicate that the reactivation process is independent of injury. Our results demonstrate Tbeta4 to be the first known molecule able to initiate simultaneous myocardial and vascular regeneration after systemic administration in vivo. Given our findings, the utility of Tbeta4 to heal cardiac injury may hold promise and warrant further investigation.

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Available from: Deepak Srivastava
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    • "Additional studies have confirmed that Thymosin b4 is a direct transcriptional target of Hand1 (Smart et al., 2010). Although the contribution of this regulatory relationship to cardiogenesis has not been defined, evidence suggests that Thymosin b4 may 488 VINCENTZ ET AL. stimulate vascular and myocardial growth while inhibiting myocardial cell death (Shrivastava et al., 2010). Disruption of Hand2 function in the mouse generates cardiac phenotypes. "
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