Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Chiba, Japan.
Circ J. 2010 Nov;74(12):2527-33. doi: 10.1253/circj.cj-10-0916. Epub 2010 Nov 12.
Epidemiological studies have shown that age is the chief risk factor for lifestyle-related diseases such as cardiovascular disease and diabetes, but the molecular mechanisms that underlie the increase in the risk of such diseases conferred by aging remain unclear. Recently, genetic analyses using various animal models have identified molecules that are crucial for aging. These include components of the DNA repair system, the tumor suppressor pathway, the telomere maintenance system, the insulin/Akt pathway, and other metabolic pathways. Interestingly, most of the molecules that influence the phenotypic changes of aging also regulate cellular senescence, suggesting a causative link between cellular senescence and aging. This review examines the hypothesis that cellular senescence might contribute to lifestyle-related disease.
流行病学研究表明，年龄是与生活方式相关的疾病（如心血管疾病和糖尿病）的主要危险因素，但导致这种疾病风险增加的分子机制尚不清楚。最近，使用各种动物模型的遗传分析已经确定了对衰老至关重要的分子。这些包括 DNA 修复系统、肿瘤抑制途径、端粒维持系统、胰岛素/Akt 途径和其他代谢途径的成分。有趣的是，影响衰老表型变化的大多数分子也调节细胞衰老，这表明细胞衰老与衰老之间存在因果关系。这篇综述探讨了细胞衰老可能导致与生活方式相关的疾病的假说。
