Su Xiaohua, Flores Elsa R
Department of Molecular and Cellular Oncology, Graduate School of Biomedical Sciences, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA.
Aging (Albany NY). 2009 Oct 21;1(10):866-9. doi: 10.18632/aging.100095.
The mechanisms controlling organismal aging have yet to be clearly defined. In our recent paper [1], we revealed thatTAp63, the p53 family member, is a critical gene in preventing organismal aging by controlling the maintenance of dermal and epidermal precursor and stem cells critical for wound healing and hair growth. In the absence of TAp63, dermal stem cells (skin-derived precursors or SKPs) in young mice are hyperproliferative. As early as one month of age, SKPs and epidermal precursor cells exhibit signs of premature aging including a marked increase in senescence, DNA damage, and genomic instability resulting in an exhaustion of these cells and an overall acceleration in aging. Here, we discuss our findings and its relevance to longevity, regenerative medicine, and tumorigenesis.
控制生物体衰老的机制尚未明确界定。在我们最近的论文[1]中,我们揭示了p53家族成员TAp63是通过控制对伤口愈合和头发生长至关重要的真皮和表皮前体细胞及干细胞的维持来预防生物体衰老的关键基因。在缺乏TAp63的情况下,年轻小鼠的真皮干细胞(皮肤衍生前体细胞或SKP)会过度增殖。早在一个月龄时,SKP和表皮前体细胞就表现出早衰迹象,包括衰老、DNA损伤和基因组不稳定显著增加,导致这些细胞耗竭以及衰老总体加速。在此,我们讨论我们的发现及其与长寿、再生医学和肿瘤发生的相关性。