Telomeres protect the chromosome ends for DNA repair and degradation activities and telomerase is the enzyme responsible for maintaining telomere length and cell self-renewal (Blackburn et al.
, 2006). Many types of in-vitro-cultured cells experience telomere exhaustion and exhibit limited proliferative capacity, a process termed replicative senescence (or Hayflick limit) (Hayflick and MOORHEAD, 1973). Telomeres and telomerase are susceptible to age-related deterioration. Studies using genetically modified animal models have demonstrated the causal links of telomere dysfunction, cellular senescence and aging. Although telomere attrition manifests during normal physiological aging, pathological telomere dysfunction provokes aging (Blackburn et al.
, 2006; Flores and Blasco, 2010) and plays a causal role in premature development of various human diseases, such as idiopathic pulmonary fibrosis (Tsakiri et al., 2007; Cronkhite et al., 2008), aplastic anaemia (Yamaguchi et al., 2005; Du et al., 2008) and dyskeratosis congenital (Armanios et al., 2005; Calado et al., 2009).
Importantly, telomere and telomerase are the main components of stem cell “ignition” mechanism, referring to uncontrolled proliferation resulting in tumor formation or, inversely, impaired self-renewal as happens in age-related tissue degeneration (Flores and Blasco, 2010). Thus, tremendous efforts have been drawn on the manipulation of telomere and telomerase to restrain cancer and delay aging. Among these, Armanios et al., and Toma´s-Loba et al., demonstrated that shortened telomere length caused tissue degeneration whereas lengthened telomere increased lifespan in mice (Armanios et al., 2009; Tomás-Loba et al.
, 2008). Moreover, normal physiological aging in mice can be delayed by systemic viral transduction of telomerase (Bernardes de Jesus et al., 2012) and reactivation of telomerase in aged telomerase-deficient mice showing reverted premature aging phenotypes in testes, spleens, and intestines (Jaskelioff et al., 2011).