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24 cze 2014 · Preferential accumulation of telomere-dysfunctional senescent cells in nfkb1−/− tissues is blocked by anti-inflammatory or antioxidant treatment of mice, and this rescues tissue...
- Mice with hyper-long telomeres show less metabolic aging and longer ...
Hyper-long telomere mice are lean and show low cholesterol...
- Mice with hyper-long telomeres show less metabolic aging and longer ...
17 paź 2019 · Hyper-long telomere mice are lean and show low cholesterol and LDL levels, as well as improved glucose and insulin tolerance. Hyper-long telomere mice also have less incidence of cancer and...
Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial biogenesis and function, decreased gluconeogenesis, cardiomyopathy, and increased reactive oxygen species.
1 lis 2023 · Telomeres are shortened after each cell division due to end-replication problem. In critical situations, they activate damage pathways leading to cell proliferation arrest, cellular senescence, and apoptosis [1]. The activity of telomerase is low in somatic cells, but significantly increased in germ cells, immortalized cells, and tumor cells.
11 kwi 2023 · Regardless of the potential off-target effects of siRNAs, these data support a role of TERT in glucose control in human skeletal muscle in the absence of telomere dysfunction (normal telomere lengths). Mice already vulnerable to oxidative stress undergo rapid vascular ageing after Pgc1α knockout.
Based on this notion, we tested the effects of a telomerase gene therapy in adult (1 year of age) and old (2 years of age) mice. Treatment of both groups of mice with an AAV of wide tropism expressing mouse telomerase (mTERT) demonstrated remarkable beneficial effects on health and fitness, improving several molecular biomarkers of aging.
In the context of telomere biology, dysfunctional telomeres induce the accumulation of telomeric dilncRNA and DDRNA (cumulatively referred here as tncRNA). tncRNA targeting with ASOs (tASOs) selectively inhibited DDR at telomeres, as demonstrated in cultured cells and in mice, where they also reduced markers of cellular senescence and apoptosis ...