New Delhi: Researchers have found that a naturally occurring molecule in the body plays a stress-reducing role, a discoverywhich they said could lead to new drugs and treatment for metabolic disorders and ageing.
Researchers from The University of Queensland looked at microRNAs, which bind to genes and prevent them from being over-activated.
The study published in the journal Nature Communications investigated damage to mitochondria — the energy powerhouse of a cell that makes muscles function, neurons to fire, among other processes in the body.
“MicroRNAs have many different functions, but this is the first time it has been shown that they regulate mitochondrial stress pathways and prevent the spread of stress signals to other cells and tissues throughout the body,” said author Steven Zuryn, a molecular geneticist at the University of Queensland.
“Damage to the mitochondria accrues over time and is closely associated with metabolic disorders and diseases of ageing including neurodegeneration, cancer and diabetes, as well as ageing itself,” Zuryn said.
The study looked at a specific microRNA, called ‘miR-71’, in Caenorhabditis elegans worm models or C. elegans.
Zuryn said the microRNAs lower chronic stress in the body and protect cells. “Our research implies that we could design highly specific and deliverable microRNAs that target these same genes in humans, thereby reducing the intensity and spread of damaging chronic stress signals.”
“We’re not necessarily aiming to develop an anti-ageing drug, but an understanding of the deep underlying mechanisms of these processes may one day lead to this outcome,” he said.
The authors said these findings open the possibility that metabolic disorders could be “ameliorated by limiting the overactivation of mitochondrial stress responses through targeted small RNAs”.
MicroRNAs were discovered in C. elegans worms about 30 years ago and have since been shown to be important in human health and disease — the discovery was awarded the Nobel Prize in Physiology or Medicine in 2024.
