Smart Nicola, Riley Paul R
Molecular Medicine Unit, UCL-Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Future Cardiol. 2012 Jan;8(1):53-69. doi: 10.2217/fca.11.87.
The mammalian heart loses its regenerative capacity during early postnatal stages; consequently, individuals surviving myocardial infarction are at risk of heart failure due to excessive fibrosis and maladaptive remodeling. There is an urgent need, therefore, to develop novel therapies for myocardial and coronary vascular regeneration. The epicardium-derived cells present a tractable resident progenitor source with the potential to stimulate neovasculogenesis and contribute de novo cardiomyocytes. The ability to revive ordinarily dormant epicardium-derived cells lies in the identification of key stimulatory factors, such as Tβ4, and elucidation of the molecular cues used in the embryo to orchestrate cardiovascular development. myocardial infarction injury signaling reactivates the adult epicardium; understanding the timing and magnitude of these signals will enlighten strategies for myocardial repair.
哺乳动物心脏在出生后早期阶段丧失其再生能力;因此,心肌梗死幸存者因过度纤维化和适应性重塑而面临心力衰竭风险。因此,迫切需要开发用于心肌和冠状血管再生的新疗法。心外膜衍生细胞是一种易于处理的常驻祖细胞来源,具有刺激新生血管形成和产生新生心肌细胞的潜力。激活通常处于休眠状态的心外膜衍生细胞的能力在于识别关键刺激因子,如Tβ4,并阐明胚胎中用于协调心血管发育的分子线索。心肌梗死损伤信号会重新激活成年心外膜;了解这些信号的时间和强度将为心肌修复策略提供启示。