ELN regulates cellular senescence: Emerging hypothesis for a non-canonical role.

Abstract

Elastic fibers are well-known extracellular matrix components that are essential for elastic properties and thus function of many tissues. Tropoelastin is encoded by the ELN gene which is the main component of the elastic fibers. Elastic fibers decrease with aging and this decrease is proposed to contribute to this process. Senescent cells, cells that stop to proliferate and that instruct their microenvironment, accumulate with aging and promote it. Until recently, whether ELN expression and function is linked to cellular senescence was unknown. Here we will comment and extend recent results supporting a function of the ELN gene in protecting cells from cellular senescence. We will also discuss hypotheses on mechanisms by which ELN could regulate cellular senescence, and especially a hypothesis that involves a non-canonical function of ELN regulating the mitochondrial respiratory chain activity, thereby controlling oxidative stress and cellular senescence. These findings provide critical insights into the molecular and cellular processes potentially underlying the phenotypes driven by ELN deletion in the context of aging.