人们都知道锻炼身体可以促进新陈代谢,有益于心血管健康,但此前科学家对运动究竟如何影响心脏 却所知甚少。美国哈佛大学医学院的研究人员日前报告说,他们首次从分子水平发现运动有益心脏健 康的机理,这一发现将有助于开发出治疗心血管疾病的新疗法。 研究人员通过小鼠实验发现,经常运动可以使小鼠体内的C/EBPβ转录因子水平显著下降,其结果会促 进小鼠心脏肌肉细胞增殖,有益于心脏生长。此外,研究人员还发现,体内C/EBPβ水平较低的小鼠对 心力衰竭具有抵抗能力。 研究人员表示,这项研究对心脏肌肉再生的潜力有了深入理解。参与研究的哈佛大学医学院教授安东 尼·罗森茨魏希表示,通过这项研究可以开发出针对那些无法运动的心脏病患者的疗法。 这项研究成果发表在新一期美国《细胞》杂志上。 C/EBPβ Controls Exercise-Induced Cardiac Growth and Protects against Pathological Cardiac Remodeling Cell, Volume 143, Issue 7, 1072-1083, 23 December 2010 10.1016/j.cell.2010.11.036 Authors Pontus Boström, Nina Mann, Jun Wu, Pablo A. Quintero, Eva R. Plovie, Daniela Panáková, Rana K. Gupta, Chunyang Xiao, Calum A. MacRae, Anthony Rosenzweig, Bruce M. SpiegelmanSee Affiliations Highlights Endurance exercise of mice induces cardiomyocyte proliferation Endurance exercise causes a reduction of C/EBPβ expression and an increase of CITED4 Reduction of C/EBPβ in vitro induces cellular hypertrophy and proliferation via CITED4 Genetic reduction of C/EBPβ in vivo results in a phenocopy of the exercised heart Summary The heart has the ability to grow in size in response to exercise, but little is known about the transcriptional mechanisms underlying physiological hypertrophy. Adult cardiomyocytes have also recently been proven to hold the potential for proliferation, a process that could be of great importance for regenerative medicine. Using a unique RT-PCR- based screen against all transcriptional components, we showed that C/EBPβ was downregulated with exercise, whereas the expression of CITED4 was increased. Reduction of C/EBPβ in vitro and in vivo resulted in a phenocopy of endurance exercise with cardiomyocyte hypertrophy and proliferation. This proliferation was mediated, at least in part, by the increased CITED4. Importantly, mice with reduced cardiac C/EBPβ levels displayed substantial resistance to cardiac failure upon pressure overload. These data indicate that C/EBPβ represses cardiomyocyte growth and proliferation in the adult mammalian heart and that reduction in C/EBPβ is a central signal in physiologic hypertrophy and proliferation. http://www.cell.com/abstract/S0092-8674(10)01358-9