Credits By: NOVOS
Scientists from The University of Queensland have uncovered a novel anti-aging role within a protein deep within human cells.
Associate Professor Steven Zuryn and Dr. Michael Dai, affiliated with the Queensland Brain Institute, have made a significant revelation: a protein named ATSF-1 regulates a delicate equilibrium between generating fresh mitochondria and rectifying damaged ones.
The Interplay Between Mitochondria and Aging Mitochondria, possessing their distinct DNA, generate cellular energy essential for biological processes. However, the detrimental byproducts stemming from this energy production contribute to the pace at which cellular aging occurs.
“In circumstances of stress, particularly when mitochondrial DNA sustains damage, the ATSF-1 protein prioritizes repair activities, thereby endorsing cellular vitality and extending longevity,” elaborates Dr. Zuryn.
Dr. Zuryn parallels this relationship and a race car necessitating a pit stop.
“Much like a race car requires a pit stop for repairs, ATSF-1 acts decisively to prompt a ‘pit stop’ for the cell when a mitochondrial repair is required,” he explains.
Mitochondria in Action: The C. elegans Model Employing C. elegans, or roundworms, as a model organism, the researchers observed the impact of ATFS-1 manipulation. Elevating its functionality distinctly boosted cellular well-being, resulting in enhanced longevity of the worms’ agility.
“While their lifespan wasn’t extended, their aging process manifested in improved health,” notes Dr. Zuryn.
The Nexus with Age-Related Disorders Dr. Zuryn stresses, “Malfunctioning mitochondria stand as the linchpin of numerous human maladies, encompassing prevalent age-related conditions such as Parkinson’s and dementia.”
The Significance for Age-Related Ailments: “Our discovery could potentially hold promising prospects for fostering healthy aging and catering to individuals grappling with hereditary mitochondrial disorders.”
Delving into the mechanics of cellular repair represents a pivotal stride toward identifying viable interventions aimed at staving off mitochondrial impairment.
“Our objective revolves around elongating the functional capacities of tissues and organs that typically wane during aging. This involves comprehending the role deteriorating mitochondria play in driving this progression,” underscores Dr. Dai.
Gazing into the Future, Dr. Dai envisions, “We might ultimately formulate strategies to sustain the health of mitochondrial DNA over an extended period, thereby augmenting our overall quality of life.”
This breakthrough study has been published in the esteemed scientific journal Nature Cell Biology.
