Exact(36)
SIRT1, being the most extensively experimented sirtuin with regards to aging and longevity, has triggered interest in scientific communities to develop small molecule activators or drugs in amelioration of a wide range of aging disorders.
Taken together, our study compares and contrasts the distinct pathologies underpinning the two premature aging disorders, and provides reliable stem-cell based models to identify new therapeutic strategies for pathological and physiological aging.
In this scenario, premature aging disorders in humans and the various animal model systems recapitulating the phenotypes of accelerated aging and cellular senescence constitute a major area of interest in understanding the intricacies of the process of aging.
A potentially successful approach involves the analysis of naturally occurring aging disorders [ 1, 2].
According to our hypothesis premature aging disorders as well as normal aging should share features with mitochondrial disease.
These findings pave the way to the development of therapeutic strategies against epigenetic modifier enzymes for the treatment of metabolic and aging disorders [ 121- 123].
Similar(24)
Alzheimer's disease (AD) is an aging disorder that leads to memory loss.
We suggest that PABPN1 levels regulate muscle cell aging and OPMD represents an accelerated muscle aging disorder.
Hutchinson Gilford progeria syndrome (HGPS, OMIM 176670) is a rare segmental premature aging disorder associated with rapid growth deceleration in childhood (Gordon et al., 2014).
Hutchinson Gilford progeria syndrome (HGPS, OMIM 176670) is a rare multisystem childhood premature aging disorder linked to mutations in the LMNA gene.
Werner Syndrome (WS) is an autosomal recessive segmental aging disorder associated with a marked predisposition to cancer and vascular disease [ 1, 2].
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