摘要
Heart regeneration is a promising strategy to prevent cardiac injury and protect against heart failure.^(1,2,3)Distinguishing from adult mammals,neonatal mouse heart can regenerate completely after cardiac injury,such as apical resection(AR)or myocardial infarction(MI).Our previous study reveals that acute inflammation is essential for initiation of neonatal mouse heart regeneration,4 providing an insight to understand the role of immune system in cardiac repair.Macrophage is a prominent inflammatory cell in injured heart during acute immune response;5 here we revealed that genetically deletion of CD11b-positive macrophages in CD11bDTR mice with diphtheria toxin(DT)administration led the suspense of neonatal heart regeneration after AR injury.We transplanted cardiac macrophages sorted from AR-injured neonatal mouse hearts into MI-injured adult mice and found that transfusion of neonatal mouse cardiac macrophages facilitated cardiac repair and enhanced cardiomyocyte proliferation effectively,which served a potential intervention to improve prognosis of patients suffering cardiac diseases.
基金
This work was supported by CAMS Innovation Fund for Medical Sciences(CIFMS,2016-I2M-1-015)
the National Key Research and Development Project of China(2019YFA0801500)
the National Natural Science Foundation of China(NSFC:81970243,81770308)
Beijing Natural Science Foundation(7172183,7182140)
and Chinese Academy of Medical Sciences Talent Fund(2018RC310005).
