Scientists have discovered an unknown genetic mechanism of cell metabolism that becomes increasingly dysfunctional with aging.

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Researchers at the École Polytechnique Fédérale de Lausanne (EPFL) in Switzerland suggest that their findings could lead to new targets for treatments to combat aging and age-related conditions.

Their discovery concerns a protein that alters the function of mitochondria, which are the tiny power units inside cells that give them their energy.

The EPFL team found that brain and muscle tissue from aged animals had high levels of the protein, which is called pumilio RNA binding family member 2 (PUM2).

A study paper in the journal Molecular Cell describes how aging induces higher levels of PUM2, which, in turn, reduce levels of another protein called mitochondrial fission factor (MFF).

MFF helps cells break large mitochondria into smaller units and clear them away. The tissue samples from the aged animals also had lower levels of MFF.

The researchers suggest that as animals age, the PUM2/MFF pathway becomes more and more dysregulated.

As PUM2 levels rise, they bring down levels of MFF. The result is that cells become increasingly unable to break up and clear away smaller mitochondria. As time goes by, cells and tissues accumulate more and more large, unhealthy mitochondria.