Mitochondrial protein associated with greater longevity in rats, reveals Japanese study.
A team of researchers in Japan has identified a possible key player in the biology of aging: the mitochondrial protein COX7RP.
According to a study in Aging Cell in November, high levels of this protein in rats were associated with a healthy life extensionby reinforcing the energy efficiency of mitochondria, the cellular structures responsible for energy production.
In recent years, research on aging has moved away from the simple idea of “living longer” and towards a different objective: increasing “healthspan“, that is, the years in which people remain healthy, autonomous and active, with fewer age-related diseases. In this context, mitochondria emerge as a central target, since the loss of mitochondrial performance has been linked to aging and metabolic and degenerative pathologies.
Energy production in mitochondria depends on a set of molecular structures, known as respiratory chain complexes, which allow the flow of electrons and protons necessary to generate ATP (adenosine triphosphate), the “energy currency” of the cells. It has been known for decades that these complexes can group together into larger, flexible formations — so-called supercomplexes — that are theoretically more efficient.
But direct evidence that this arrangement has measurable health benefits, particularly in animals, has been limited—possibly until now.
The team led by Satoshi Inouefrom the Tokyo Metropolitan Institute for Geriatrics and Gerontology, focused on COX7RP, a protein that promotes the assembly of these supercomplexes. To test its impact, researchers created transgenic mice that expressed higher levels of COX7RP throughout life, explains .
The results indicate that these animals lived, on average, 6.6% longer than unmodified mice. In addition to longevity, it was observed metabolic improvementsincluding greater insulin sensitivity and better glycemic control, as well as more favorable lipid profiles, with a reduction in triglycerides and total cholesterol. The transgenic mice also showed greater muscular endurance and less fat accumulation in the liver.
At the cellular level, the tissues of these animals showed greater formation of supercomplexes and increased ATP production. In white adipose tissue, there were also signs compatible with slower aging: higher levels of (a coenzyme associated with metabolism), lower production of reactive oxygen species (ROS) and reduced markers of cellular senescence, including β-galactosidase.
Genetic analyzes in aged rats suggested even less activation of genes linked to inflammation associated with aging, including components of the so-called senescence-associated secretory phenotype (SASP).
The authors argue that reinforcing mitochondrial energy efficiency can delay metabolic changes typical of age and point to the possibility that, in the future, supplements or drugs capable of enhancing the assembly and function of these supercomplexes may contribute to increasing healthy longevity.
