Matt Elliott 
A single gene switch controls how infant heart cells generate energy, regulating a critical metabolic transition after birth. The switch gradually shifts mitochondrial function from glucose reliance to the balanced metabolism of mature hearts.
Damaged mitochondria release DNA fragments into the blood. Researchers are investigating whether measuring these fragments could detect brain disease progression before symptoms appear.
Researchers have shown that transplanting healthy mitochondria into damaged cells can restore energy production and improve cell survival in laboratory and animal studies. The approach could theoretically address acute injuries where cells die from energy failure, though questions remain about scalability and long-term effects.
As we age, stem cells gradually lose their capacity to divide and repair tissue damage. Scientists have identified multiple cellular mechanisms driving this decline, from mitochondrial dysfunction to changes in genetic signalling.
When you stop eating, your cells shift into maintenance mode. Autophagy, a cellular recycling process, intensifies during fasting periods, breaking down damaged proteins and organelles for reuse.
Iron nanoparticles from air pollution trigger a cascade of free radical damage inside cells, overwhelming their natural defence systems. This oxidative stress response reveals how sensitive cellular machinery is to metal contamination.
In laboratory studies, the red pigment astaxanthin appears to reactivate death signals that liver cancer cells normally suppress. Researchers are investigating how the molecule influences the signalling pathways that allow cancer cells to survive.
Smoking delivers trillions of free radicals directly into your bloodstream, overwhelming the antioxidant defences that protect retinal cells. Research shows smokers accumulate retinal oxidative damage at rates decades ahead of non-smokers, leading to vision loss and disease earlier in life.
Preclinical research shows that chronic oxidative stress accelerates ageing in the hippocampus, the brain region responsible for memory formation. The effect appears to stem from the hippocampus operating near the limit of its antioxidant defences due to high metabolic demands.
Hyperspectral cameras combined with AI algorithms can detect oxidative stress in cells minutes to hours before conventional methods identify damage. This non-invasive approach reads the spectral fingerprints of stressed cells, opening new possibilities for early detection in research and potentially in clinical settings.
When T cells fight infection, metabolic stress leaves chemical marks on their DNA and proteins that persist for months or years. These marks may be how immune cells encode lessons from past challenges into their structure.
Cells control mitochondrial fragmentation through a signalling pathway involving PKCδ and Drp1 proteins. Researchers are uncovering how this mechanism helps cells survive stress while maintaining energy production.