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24 cze 2014 · Senescent cells harbouring dysfunctional telomeres, which are recognized by persistent telomere-associated DNA damage foci (TAF), accumulate even in tissues of ageing mice with long telomeres...
19 paź 2022 · Telomere restoration therapy extends the lifespan of aged mice by 20%. Our telomeres shorten as we age, causing our DNA repair systems to malfunction. In response, affected cells convert to a senescent state, secreting molecules known as the senescence-associated secretory phenotype (SASP).
1 lis 2023 · The link between telomere dysfunction, hallmarks of aging and incidence of age-related diseases has spawned interest in telomerase recovery therapy as a potential anti-aging strategy.
24 sty 2024 · An in vivo study investigated the influence of telomere length on health in mice derived from embryonic stem cells with hyper-long telomeres. The mice with hyper-long telomeres exhibited reduced DNA damage with aging, improved metabolic markers such as lower LDL levels, improved glucose and insulin tolerance, decreased cancer incidence, and ...
Here Jurk et al. use a mouse model of chronic, low-grade inflammation to support a model by which such inflammation promotes a vicious cycle of oxidative stress, telomere dysfunction and cell senescence that accelerates the ageing process. Many age-related diseases and ageing itself are closely associated with low-level chronic inflammation 1, 2.
14 lip 2015 · Here, we generate two independent mouse models that develop IPF owing to either critically short telomeres (telomerase-deficient mice) or severe telomere dysfunction in the absence of telomere shortening (mice with Trf1 deletion in type II alveolar cells). We show that both mouse models develop pulmonary fibrosis through induction of telomere ...
30 sty 2018 · We show here that telomerase expression using AAV9 vectors shows therapeutic effects in a mouse model of pulmonary fibrosis owing to a low-dose bleomycin insult and short telomeres. AAV9 preferentially targets regenerative alveolar type II cells (ATII).
