From the Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Centre (CNIO), Madrid, Spain.
Circ Res. 2018 Sep 14;123(7):787-802. doi: 10.1161/CIRCRESAHA.118.312202.
Telomeres, the protective ends of linear chromosomes, shorten throughout an individual's lifetime. Accumulation of critically short telomeres is proposed to be a primary molecular cause of aging and age-associated diseases. Mutations in telomere maintenance genes are associated with pathologies referred to as or telomeropathies. The rate of telomere shortening throughout life is determined by endogenous (genetic) and external (nongenetic) factors. Therapeutic strategies based on telomerase activation are being developed to treat and prevent telomere-associated diseases, namely aging-related diseases and telomeropathies. Here, we review the molecular mechanisms underlying telomere driven diseases with particular emphasis on cardiovascular diseases.
端粒是线性染色体的保护性末端，会随着个体的一生而逐渐缩短。端粒长度过短被认为是衰老和与年龄相关疾病的主要分子原因。端粒维持基因的突变与被称为端粒体病的病理学有关。端粒在整个生命周期中的缩短速度取决于内源性（遗传）和外源性（非遗传）因素。基于端粒酶激活的治疗策略正在被开发用于治疗和预防与端粒相关的疾病，即与衰老相关的疾病和端粒体病。在这里，我们回顾了端粒驱动疾病的分子机制，特别强调了心血管疾病。
