All of these different mitochondrial signaling pathways
can regulate each other, but how these factors cooperate to promote
cellular senescence, and whether these pathways are conserved in all
senescent cells still remains unclear. Nonetheless, studying these
different factors can provide new insights into the mechanisms involved
in mitochondrial dysfunction-associated senescence. Because both
mitochondrial defects and cellular senescence accumulate with age,
linking the pathways involved in these two phenomena may help us
understand the biology of aging, providing new potential targets to
treat age-related diseases.