BIMR logoA new research conducted at Burnham Institute for Medical Research has claimed that it has apparently discovered the preserved protein d4eBP modulates cardiac aging in Drosophila i.e. fruit flies. The research team also discovered that d4eBP, which apparently attaches to the protein dEif4e, may shield heart function against aging.

This research may apparently improve our understanding of the TOR and FoxO signaling pathway and could offer a more definite objective for additional research into cardiac aging. As the TOR and FoxO genes are said to be preserved between Drosophila and humans, this work may result in novel, tissue-specific techniques to guard the heart.

A large amount of research has illustrated that changing the expression of particular genes may lengthen the lifespan of a variety of organisms. Over expression of dFoxO and condensed expression of dTOR both apparently work to lengthen the lifespan of Drosophila. But, researchers apparently wanted to examine the mechanisms behind these pathways, as well as how these signaling pathways may influence aging in definite tissues. In this case it appears to concern the heart.

Rolf Bodmer, Ph.D., who directs Burnham’s Development and Aging Program, commented, “The relationships between these genes are very complex. We wanted to analyze how two opposing genes function and control their downstream effectors, and we wanted to understand how these aging factors apply to a specific organ.”

The Bodmer laboratory, in partnership with the laboratory of Sean Oldham, Ph.D., a researcher in TOR signaling, apparently changed the expression levels of dTOR pathway components in heart tissue and supposedly examined the stress response of the hearts. Increased dTOR activation may lead to higher failure rates, while decrease in dTOR activity may encourage more young hearts. Observing that upregulated dFoxO and downregulated dTOR could result in similar consequences, the laboratory searched for downstream factors that were apparently predisposed by both pathways. One option was d4eBP, which could decrease messenger RNA translation by attaching to dEif4e. It was discovered that increased d4eBP levels apparently formed the same healthier hearts as reduced dTOR activity, while increased dEif4e levels could lead to higher failure rates.

The team also illustrated that when dTOR and its opposed effecter d4eBP were apparently co-expressed, the hearts apparently did not vary considerably from when d4eBP was expressed by itself, which may signify that there may be a straight signaling path from dTOR to d4eBP/dEif4e. These new results also bring about the interesting biological concept that could change inTOR-dependent mRNA translation factors namely d4eBP and dEif4e influence the age-dependent functional performance of the heart.

This research was published in the Aging Cell.