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Since decreased TOR/insulin/IGF-1 signaling extends life span, p53 may regulate aging and longevity through its down-regulation of the signaling of these two critical pathways.
Despite these important discoveries, additional alleles that may regulate aging in humans and allow a minority of the population to attain extreme old age have likely yet to be identified.
Also, it was suggested that hypothalamic SIRT1 may regulate aging [ 5].
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These results strongly suggest that this increased SIRT1 may contribute to cellular lifespan extension and aging impairment, which may regulate age-related genes such as p16 due to its epigenetic and potentially genetic effects.
Studies with nematodes [ 35- 38], Drosophila [ 39- 42], and rodents [ 43- 49] suggest that the molecular processes that regulate aging and longevity may be similar to those that regulate resistance to oxidative stress.
Studies with nematodes [ 26- 29], Drosophila [ 30- 33], and rodents [ 34- 40] suggest that the molecular processes that regulate aging and longevity may be similar to those that regulate resistance to oxidative stress.
Physiological and other approaches indicate that mitochondria may also regulate ageing.
Given that Sir2 family members regulate aging, the FOXO/SirT regulatory network may be a key factor for understanding the relationship between oxidative stress and life span [ 9].
A similar gene in humans is known to regulate aging.
Moving further, considering that modules regulating aging in model systems may not be related to human aging, mouse consensus modules were matched against human based on homologs.
Many conserved miRNAs along with a few species-specific miRNAs become more abundant and may regulate reproduction or aging.
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