A protein called ATSF-1 found in human cells may contribute to anti-aging, according to researchers at the University of Queensland. ATSF-1 regulates the equilibrium between generating new mitochondria and repairing damaged ones.
Unique DNA in mitochondria generate energy for biological functions
Mitochondria, the cellular powerhouses possessing their unique DNA, generate energy to fuel biological operations; however, the detrimental byproducts of this mechanism are implicated in accelerating cellular aging. The transcription and maintenance of the mitochondrial genome (mtDNA) necessitate distinct enzymatic functions that may potentially engage in steric competition, implying an enduring trade-off between these dual processes throughout an individual’s lif
Queensland Brain Institute’s Dr Steven Zuryn said that during stress , after mitochondrial DNA destruction, the priority for the ATSF-1 is repair to stimulate cellular growth and longevity. It functions as a central molecular hub for regulating the equilibrium between mitochondrial genome expression and upkeep. The researcher likened the relationship to a F1 car requiring pitstop. Dr Zuryn explained that ATSF-1 makes the call when a pistop is necessary for the mitochondria to carry out repairs.
The scientists examined ATFS-1 within C. elegans, commonly known as roundworms, and observed that bolstering its capabilities resulted in the improvement of cellular well-being, leading to increased longevity of the worms’ vitality and agility.
Mitochondrial dysfunction responsible for most diseases
According to Dr. Zuryn hey did not experience extended lifespan but they exhibited improved health as they grew older. Mitochondrial dysfunction stands as a central factor in numerous human ailments, encompassing prevalent age-associated conditions like dementia and Parkinson’s disease. The discovery may hold promising ramifications for promoting a healthier aging process and offering potential benefits for individuals afflicted with inherited mitochondrial disorders.
Comprehending the mechanisms by which cells facilitate repair represents a crucial stride in the quest to pinpoint potential strategies for mitigating mitochondrial harm.
Queensland Brain Institute’s Michael Dai said that their aim is to prolong organ and tissue functions that usually deteriorate during aging by getting insight on mitochondria’s role in the whole process. He explained that this may eventually lead to development of innovations that maintain health of mitochondria and enhance quality of life.