Cardiac repair with thymosin β4 and cardiac reprogramming factors.
Heart disease is a leading cause of death in newborns and in adults. We previously reported that the G-actin-sequestering peptide thymosin β4 promotes myocardial survival in hypoxia and promotes neoangiogenesis, resulting in cardiac repair after injury. More recently, we showed that reprogramming of cardiac fibroblasts to cardiomyocyte-like cells in vivo after coronary artery ligation using three cardiac transcription factors (Gata4/Mef2c/Tbx5) offers an alternative approach to regenerate heart muscle. We have combined the delivery of thymosin β4 and the cardiac reprogramming factors to further enhance the degree of cardiac repair and improvement in cardiac function after myocardial infarction. These findings suggest that thymosin β4 and cardiac reprogramming technology may synergistically limit damage to the heart and promote cardiac regeneration through the stimulation of endogenous cells within the heart.
Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA. dsrivastava@gladstone.ucsf.edu
Deepak
D
Srivastava
Masaki
M
Ieda
Jidong
J
Fu
Li
L
Qian
D000818:Animals; D006321:Heart / Q000187:drug effects*; D006801:Humans; D051379:Mice; D009203:Myocardial Infarction / Q000188:drug therapy*; D009206:Myocardium / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects; D012038:Regeneration / Q000187:drug effects; D013947:Thymosin / Q000627:therapeutic use*; D014945:Wound Healing / Q000187:drug effects; D000099201:Thymosin beta(4)
D013947:Thymosin; D000099201:Thymosin beta(4)