The Mighty Mitochondria

You have probably heard that mitochondria are called the “powerhouse of the cell” and yes, that’s true! These organelles produce ATP, which is the main energy supply that runs our cells. But their job doesn’t end there. Mitochondria are involved in metabolism, cell signaling, immunity, and homeostasis. However, as we age, mitochondria may not always be as efficient, and the processes through which they fuse, divide and transit can be negative impacted.

In this post, I will explain how mitochondria are formed (also known as mitochondrial biogenesis), how mitochondria functioning affects redox balance, the key to mitochondrial flexibility, and how exercise can improve the deterioration of mitochondrial function that is associated with aging. We will also explore some new peptides that have emerged recently, such as MOTS-C and SHMOOSE that are providing new insights into the protection and possibly enhancement of mitochondrial function and longevity.

The Story Behind Mitochondria

Mitochondria were first identified in 1890 by German pathologist Richard Altmann who referred to them as “bioblasts.” It was not until 1967 that scientist Lynn Margulis (then Sagan) suggested a revolutionary theory: mitochondria are the result of a capture of ancient bacteria, which explains why they have their own DNA and ribosomes.

We now know that there are more than 10 billion mitochondria present throughout the cells in the form of complex and dynamic network that control energy production, cellular efficiency, and stress protection. As a result, researchers continue to explore how mitochondrial dysfunctions are associated with diseases such as type 2 diabetes, cancer and neurodegenerative diseases.

One thing to note: Mitochondrial derived microproteins (MDPs) are similar to nuclear encoded microproteins, but they are not the same. These differences will enable us to identify new potential targets for supporting mitochondrial function, as our patients grow older and encounter age-related conditions.