How Targeting a Key Protein Can Combat Aging

Within the human body lies a little-known protein that can have a great impact on the body’s aging process. The protein in question alters the function of the powerhouse of each cell in the body that grants it energy, the mitochondria.

This protein is known as mitochondrial fission factor, or MFF. MFF has the capacity to divide larger mitochondria into smaller subunits and clear them away.

The Process Behind Fission and Fusion

Mitochondria move like bacteria by carrying out the process of fission, dividing a single entity into two or more parts, and fusion, combining uninuclear cells to form a multinuclear cell. In recent years, there have been studies to suggest that there is an imbalance in these processes. This imbalance of fusion and fission has facilitated further research on this topic. To understand how this protein can affect maturity, the actual process of aging should be understood first.

How the Body Reacts Over Time

The root causes of the changes humans go through as they naturally age is embedded within our cellular structure. As we age, tissues lose cells, and junk material known as amyloid accumulates outside of the cells. Some of the proteins outside of the cells that are vital to skin elasticity and the artery walls also gradually degrade as we grow. This happens because these specialized proteins are created early in the lifespan, and they are either recycled at a very slow rate or never recycled at all.

How Aging Is Specifically Targeted With MFF

In terms of the role that MFF plays in this process, mRNA and another protein are integrated. Messenger RNA serves as a temporary copy of information that is found in our DNA and transfers messages to the ribosomes. Another protein in the body, called Pumilio2 (PUM2), binds to mRNA molecules and represses translation of target mRNAs into proteins.

This is where MFF comes in. High levels of MFF allow for the clearance of dysfunctional mitochondria, a process referred to as mitophagy. The axis of PUM2 and MFF is not regulated as we grow, according to studies. This has shown to be the case through the examination of muscle and brain tissues of animals that had higher concentrations of PUM2 and fewer MFF proteins. This could lead to a reduction in fission of the mitochondria and mitophagy. As a result, this causes tissues to accumulate into larger organelles.

However, it has been suggested that removing PUM2 from the muscles of mice can reverse this process. The thinking behind this would be that fragmentation of the mitochondria and mitophagy would increase. A preliminary study  showed that improvement of mitochondrial function in old animals was a result of reducing PUM2 levels.

The Future of MFF Research

Numerous degenerative diseases that can be associated with increased age are linked to RNA-binding proteins. MFF mRNA is often trapped by particles that come from the condensation of PUM2. While further studies are being conducted to show the full effectiveness of the initiative, results have been promising in targeting dysfunctions related to increased age.

It has been shown that PUM2 impairs mitochondrial fission and that the PUM2/MFF axis regulates mitochondrial function. It has also been shown that depletion of PUM2 in animals has improved homeostasis of the mitochondria. Unfortunately, information on the mechanisms that truly affect the process of growing old is scarce. In spite of that, potential interventions to combat age-related issues exist in the form of fixing the cellular structure of the human body. Maturity is a natural inevitability everyone has to face, but research suggests that by intervening with MFF and PUM2, age-related complications may soon be a thing of the past.