Articles tagged with Mitochondria
Researchers developed a technique to prevent inherited mitochondrial disorders by transferring hereditary material from one egg to another. The method resulted in four healthy newborns and holds the potential for couples to have biologically their own child without defects associated with maternal mitochondria.
A study published in JBC found that mice with defective mitochondrial protein MCLK1 lived longer and aged slower than normal mice. Despite high levels of oxidative stress, their inefficient mitochondria produced less energy and fewer oxygen radicals, accumulating less damage over time.
A genetic study found that Townsend's warblers have inherited mitochondrial DNA from hermit warblers, indicating interbreeding in the past. The DNA analysis suggests that natural selection drove hermits out of their range, leaving behind genetic fingerprints.
Research on ethanol-induced gastric mucosa injury reveals the critical role of oxidative stress in energy metabolism disturbance. Elevated ethanol exposure time increases malondialdehyde content, damaging mitochondria ultrastructure.
Research at Vanderbilt University Medical Center found that genetic variation in the mitochondrial genome is associated with an increased risk of age-related macular degeneration, a leading cause of blindness in Caucasians over 50. This discovery may lead to personalized medicine and preventive treatments.
Research by Atsuko Kasahara and colleagues found that mitochondrial respiration deficiencies are associated with changed social behavior and elevated spatial memory in laboratory mice. The study suggests a potential link between mitochondrial breakdowns and mental illness in humans.
Researchers investigate natural mitochondrial DNA variation's effect on human male fertility and sperm competitiveness. They found mitochondrial mutations to be a primary cause of low sperm count and poor mobility.
Researchers at the University of Oregon have discovered zebrafish as an ideal model for studying COX deficiencies, which can lead to fatal metabolic disorders. The use of zebrafish allows scientists to visualize early stages of mitochondrial impairments and identify specific targets for potential drug therapies.
A University of Florida study found that reducing calorie intake boosts cells' ability to recycle damaged parts, leading to longer lifespans in rats. The process, called autophagy, helps remove toxic materials and recycle building blocks for new cell production.
In mice and human patients, researchers found that crippling of protective enzyme Prx2 leads to death of dopamine-producing neurons in Parkinson's disease. Activating Prx2 prevents neuronal loss, suggesting it as a beneficial target for PD treatment.
Researchers at Johns Hopkins found that cancer cells can reprogram themselves to use less oxygen and more glucose, allowing them to survive and spread. The loss of a single gene causes cancer cells to stop making mitochondria, leading to the use of fermentation for energy production.
Researchers discovered how cells fine-tune oxygen use to make do with limited availability. They found that under stress, cells replace one protein with an energy-efficient substitute to maintain power production.
Scientists from Harvard University and the University of Pittsburgh found that carbon monoxide reduces or shuts down inflammatory responses by releasing chemical signals in mitochondria. This discovery raises hopes for developing new anti-inflammatory therapies, such as low levels of inhaled carbon monoxide.
The St. Jude study found that cells shift their biochemical activities to conserve energy by increasing glucose production and recycling CoA, a key player in metabolism. The researchers also showed that PanK controls the concentration of CoA in specific locations within the cell.
The MitoChip v2.0 is a second-generation 'lab on a silicon chip' that rapidly sequences all mitochondrial DNA, accelerating research in fields like cancer diagnostics and gerontology. The new tool detected nearly three dozen variations in the non-coding D-loop region, improving its sensitivity and reproducibility.
Research reveals that differences in overall muscle efficiency cannot be explained by variations in individual mitochondria's ability to convert food energy into ATP. Instead, the findings suggest that ATP usage within the muscle plays a crucial role in determining efficiency.
A multidisciplinary team at UCI will investigate the connection between genetic variations in mitochondria and metabolic syndrome symptoms. The research may lead to new diagnostic tools and treatments for conditions like diabetes and cardiovascular disease.
Researchers found that old mitochondria are leaky, reducing ATP production and making normal activities challenging for the elderly. This inefficiency affects muscle cells' ability to produce useable energy.
Research by Yale University found that insulin-resistant individuals' mitochondria produce less ATP, a key energy molecule. This defect may explain the link between inherited type 2 diabetes risk and reduced insulin signaling.
Rising temperatures exacerbate cadmium's toxic effects on oysters, reducing their survival chances and increasing metabolic rate. As a result, future research will focus on the thermal tolerance of cold-blooded species affected by cadmium pollution.
Researchers found that excessive build-up of succinic acid in mitochondria triggers a sequence of events leading to tumour growth. The study increases understanding of molecular basis of several types of cancer, crucial for developing new prevention, diagnosis and treatment methods.
Researchers use nuclear transfer to add women's own mitochondria to eggs, preventing inherited diseases caused by mitochondrial mutations. The technique involves adding the woman's own mitochondria to her eggs, reducing controversy and potential health risks compared to using donor mitochondria.
Researchers found over 200 mitochondrial genetic fragments integrated into nuclear genome, potentially disrupting human health. These fragments, known as NUMTs, were more likely to insert themselves within active genes, causing disease.
Mitochondrial damage is a key factor in Lou Gehrig's disease, causing cells to die. The study reveals that mutant SOD1 protein clogs the transport system of mitochondria in muscle-controlling nerve cells.
Mitochondria are targeted by a mutant protein called SOD1, leading to the progressive degeneration of motor nerve cells in spinal cord. The study provides the first explanation for how this mutant protein causes ALS, a disease characterized by wasted muscles and premature death.
Researchers found that mitochondrial DNA mutations enabled early humans to adapt to colder climates, reducing the risk of diseases such as diabetes and cardiovascular disease. The study suggests a link between genetic history and current disease predispositions.
Researchers from the Smithsonian Tropical Research Institute are using a $5 million grant to study Wolbachia, a bacterium that affects insect reproduction and evolution. The team will collect insects in Panama and use molecular tools to identify Wolbachia strains and understand their effects on host organisms.
The study found a specific genetic risk factor, the J haplogroup, to be protective against Parkinson's disease, particularly in white women. The researchers also discovered that this variant is more common in people with lower incidences of the disease.
Scientists have solved the long-standing riddle of how nitroglycerin works by discovering an enzyme called mitochondrial aldehyde dehydrogenase (mALDH) that breaks down the drug. The team found that mALDH causes nitric oxide to be released from nitroglycerin, leading to tolerance in patients.
Hydrogenosomes evolved from mitochondria in response to drastic ecological changes, displaying both species-specific and conserved features. The research team found that the contents and form of hydrogenosomes differ across species, with some resembling mitochondria.
A team of researchers from Tufts University and Brigham and Women's Hospital discovered that nitric oxide plays a key role in controlling the firefly flash. The findings, published in Science, reveal how a temporary cut in mitochondrial power supply triggers the firefly's bioluminescent glow.
Researchers discovered two molecular switches, Jnk1 and Jnk2, that stimulate programmed cell death in response to UV radiation. Disrupting these genes protects cells from lethal doses of UV light, providing a promising new therapy for diseases such as strokes and heart attacks.