Altered Intercellular Communication

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Cells, as they age, show an increase in self-preserving signals that result in damage elsewhere. Altered intercellular communication with aging contributes to decline in tissue health.

Like the decline in stem cell renewal, the age-dependent changes in intercellular communication are integrated effects of the other hallmarks of aging. In particular, senescent cells trigger chronic inflammation that can further damage aging tissues.

The cdc42 GTPase pathway, in addition to the NF-κB pathway, has been shown to increase inflammation in senescent cells; in fact, knocking down cdc42 expression actually increases longevity in C. elegans. GTPases also integrate signals from cell-cell junctions, which may break down in aging tissues.

At an organ system level, the aging hypothalamus drives changes in neurohormone signaling, which in turn affects food intake and metabolism. Since the hypothalamus also regulates sleep cycles, these changes can inhibit DNA repair, exacerbating the aging phenotype.


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Hematopoetic Stem Cells (HSCs). Cdc42 and other pathways mediate signaling between aging HSCs and their niche (within the bone marrow). As HSCs age, they move further from the niche, lose cell polarity, and undergoe DNA damage. 
Did you know?
Inflammaging is defined as chronic, low-grade inflammation that is seen with aging. Inflammaging differs significantly from acute inflammation in that it is low-grade, controlled, asymptomatic, and persistent or chronic. Most age-related diseases share an inflammatory pathogenesis, making inflammatory pathogenesis, making Inflammaging a significant risk factor in our health as we age.

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