Disruption of T Cell Mitochondrial Function Produces Accelerated Aging Symptoms in Mice – Innovita Research

Disruption of T Cell Mitochondrial Function Produces Accelerated Aging Symptoms in Mice

One has to be cautious about studies in which metabolism is broken in some way, and symptoms of aging start to appear earlier as a result. Whether or not this has any relevance to normal aging is dependent on the fine details of the biochemistry involved, and can often be argued either way even by those with the most knowledge in the field.

Aging is an accumulation of damage and dysfunction in cells and tissues. Many genetic alterations and toxins that disrupt cell metabolism will lead to damage and dysfunction, and thus conditions that appear similar to those of aging. But unless it is the same forms and distribution of damage, and it never is, there may well be little to learn that will help in treating aging.

Image credit: tiburi via Pixabay (Pixabay licence)

Image credit: tiburi via Pixabay (Pixabay licence)

In today's research, the scientists involved find that deletion of TFAM from T cells in mice breaks mitochondrial function in a way that leads T cells to become highly inflammatory, pumping out signals that are known to increase the pace at which cells enter a senescent state. The mice exhibited raised levels of cellular senescence throughout the body, a characteristic attribute of older animals. Senescent cells contribute to aging via their own signaling that rouses the immune system to chronic inflammation and disrupts tissue function.

The researchers tested a few interventions that partially reversed the harms done by this genetic modification, both of which are under investigation as therapies for aging, but the data from this study cannot indicate whether or not they would be useful in normally aged mice or humans. It is an example of producing a greatly exaggerated form of a dysfunction that does exist in normal aging, but to a lesser degree.

That aside, I think that this work does succeed in emphasizing the importance of mitochondrial function, chronic inflammation, and cellular senescence in aging. Scientific programs seeking to address the issue of mitochondrial decline in aging could certainly benefit with greater funding and support.

Approaches to suppress chronic inflammation are popular and very well funded, but still somewhat stuck in the paradigm of blocking inflammatory signals, a strategy that has significant side-effects, rather than focusing on the root causes of overactivation of the immune system. At least we can say that work on clearing senescent cells from old tissues is finally forging ahead, better late than never.

Link: Defective immune cells could make us old

Source: Fight Aging!