Why do we age? It’s a simple question with a not-so-simple answer. But with the help of modern biotechnology, scientists have been able to slowly piece together the biochemical basis of this long-held mystery.
Our cells are like tiny molecular factories, working to carry out all of the essential processes our bodies need to survive. However, like factories, the machinery in our cells gets worn out over time, which is what causes our cells to age.
Our cellular machinery is split into different substations, called organelles. And, when it comes to aging, two organelles are particularly important: a) the mitochondria—the energy-producing powerhouses of the cell, and; b) the lysosomes—the cell’s internal garbage disposal station.
During the energy-making process, mitochondria can produce dangerous waste products, which build up over time and damage our DNA. Lysosomes, meanwhile, contain a soup of digestive enzymes that breakdown worn-out cellular components. If the lysosomes themselves become damaged, these enzymes can leak out into the rest of the cell and cause havoc on the remaining healthy cellular components. Therefore, damage to either of these cellular stations has been associated with aging, cell death and many age-related diseases.
Clearly, keeping these organelles in ship shape is essential for the health and longevity of our cells. But exactly how our bodies maintain and repair these cellular substations is still unknown.
That may all be about to change. In a recent study, published in the journal Proceedings of the National Academy of Sciences, researchers from Osaka University in Japan have identified a protein that plays an important role in the maintenance of these molecular machines, and their disposal should they go wrong.
In previous research, scientists had identified a cellular switch involved in the maintenance and removal of damaged mitochondria and lysosomes. However, exactly how this molecular switch, called TFEB, was able to interact with these organelles was unclear.
Now, the team at Osaka have discovered that TFEB acts by increasing the production of a protein called HKDC1, which increases in concentration in the cell during times of mitochondrial and/or lysosomal stress. But then the question remains: what does this protein actually do?
Together with TFEB, HKDC1 is involved in the controlled removal of damaged mitochondria—in other words, it helps take out the mitochondrial trash. HKDC1 also appears to play an important role in allowing cross-talk between these two cellular structures, supporting the repair of damaged lysosomes.
Dysfunction of either of these repair pathways is linked to aging and age-related disease, suggesting that HKDC1 may offer a useful target for anti-aging treatments in the future.
