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C1q蛋白促进衰老


[ 作者:Admin     来源:运动解剖学课程网站      点击数:     更新时间:2013/09/08     文章录入:Admin ]



     

       C1q蛋白在高龄实验鼠体内含量远高于幼鼠,如果使实验鼠体内不再产生C1q蛋白,其患上动脉硬化等疾病的风险会大大降低。研究发现,2岁以上高龄实验鼠(老鼠平均寿命约2岁半)血液中C1q蛋白含量较出生2月幼鼠高5倍,而且C1q蛋白在心脏和肺等多个脏器内都会增加。进一步研究表明,C1q蛋白会扰乱组织再生,如果C1q蛋白的量过剩,就会促进衰老。通过基因敲除,使小鼠不能产生C1q蛋白,则小鼠肌肉等组织的再生变得非常活跃,且心力衰竭、动脉硬化、糖尿病等症状也得到改善。人体也存在C1q蛋白,如果能够开发出遏制C1q蛋白发挥作用的药物,有可能预防和治疗上述疾病。但由于C1q蛋白对人体也有许多积极作用,因此如何平衡利弊将是一大难题。

                                    Complement C1q Activates Canonical Wnt Signaling and Promotes Aging-Related Phenotypes

      Wnt signaling plays critical roles in development of various organs and pathogenesis of many diseases, and augmented Wnt signaling has recently been implicated in mammalian aging and aging-related phenotypes. We here report that complement C1q activates canonical Wnt signaling and promotes aging-associated decline in tissue regeneration. Serum C1q concentration is increased with aging, and Wnt signaling activity is augmented during aging in the serum and in multiple tissues of wild-type mice, but not in those of C1qa-deficient mice. C1q activates canonical Wnt signaling by binding to Frizzled receptors and subsequently inducing C1s-dependent cleavage of the ectodomain of Wnt coreceptor low-density lipoprotein receptor-related protein 6. Skeletal muscle regeneration in young mice is inhibited by exogenous C1q treatment, whereas aging-associated impairment of muscle regeneration is restored by C1s inhibition or C1qa gene disruption. Our findings therefore suggest the unexpected role of complement C1q in Wnt signal transduction and modulation of mammalian aging.