Longer-Lived Mammals Tend to Have Lower Expression of Inflammation-Related Genes

Researchers here make a few interesting observations on gene expression data from a range of mammalian species with very different life spans. Longer-lived species exhibit weaker inflammatory responses and more effective DNA repair, for example. Chronic inflammation is a feature of aging, as the immune system reacts to molecular damage and the presence of increasing numbers of senescent cells. Unresolved inflammatory signaling is disruptive to cell behavior and tissue function throughout the body, and is implicated in the onset and progression of all of the common age-related conditions.

Researchers compared the gene expression patterns of 26 mammalian species with diverse maximum lifespans, from two years (shrews) to 41 years (naked mole rats). They identified thousands of genes related to a species' maximum lifespan that were either positively or negatively correlated with longevity. They found that long-lived species tend to have low expression of genes involved in energy metabolism and inflammation; and high expression of genes involved in DNA repair, RNA transport, and organization of cellular skeleton (or microtubules).

Previous researchhas shown that features such as more efficient DNA repair and a weaker inflammatory response are characteristic of mammals with long lifespans. The opposite was true for short-lived species, which tended to have high expression of genes involved in energy metabolism and inflammation and low expression of genes involved in DNA repair, RNA transport, and microtubule organization.

When the researchers analyzed the mechanisms that regulate expression of these genes, they found two major systems at play. The negative lifespan genes - those involved in energy metabolism and inflammation - are controlled by circadian networks. That is, their expression is limited to a particular time of day, which may help limit the overall expression of the genes in long-lived species. On the other hand, positive lifespan genes - those involved in DNA repair, RNA transport, and microtubules - are controlled by what is called the pluripotency network. The pluripotency network is involved in reprogramming somatic cells into embryonic cells, which can more readily rejuvenate and regenerate, by repackaging DNA that becomes disorganized as we age.

Link: https://www.rochester.edu/newscenter/the-secret-to-a-longer-lifespan-gene-regulation-holds-a-clue-523672/

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