Articles tagged with Mitochondria
Researchers investigated the role of mitochondria in adrenoleukodystrophy, a disease causing spinal cord degeneration. They found that a diabetes drug, pioglitazone, halted nerve fibre degeneration by preventing mitochondrial loss and oxidative stress.
A study published in PNAS reveals how disrupted cellular energy metabolism contributes to the development of Alzheimer's disease. In early-stage Alzheimer's, amyloid-beta-peptide accumulation disrupts mitochondrial function, leading to over-accumulation of calcium and neuronal death.
Researchers found that resistance training promotes the growth of white muscle, which helps regulate blood glucose levels. The study also identified potential drug targets for obesity and metabolic disease.
A team of EPFL researchers has identified a key step in the manufacture of red blood cells, revealing the subtle regulatory mechanisms that direct their birth. The discovery highlights the importance of mitophagy, the elimination of mitochondrial respiratory apparatus, and its modulation by KRAB-containing zinc finger proteins and KAP1.
Scientists at Brown University and Indiana University have traced mitochondrial-nuclear incompatibility in fruit flies to individual nucleotide mutations, revealing how the genetic double whammy makes flies sick. The study highlights the importance of considering both genomes in understanding metabolic diseases.
Research by Monash University scientists found that genetic variation in mitochondrial DNA can predict male life expectancy, but not female. The study suggests that these mutations, which affect males' aging speed and lifespan, are passed down from mothers due to the unique inheritance pattern of mitochondria.
Researchers at Johns Hopkins have defined the structure of mitoKATP, a potassium channel protecting against tissue damage due to heart attacks and strokes. The discovery improves heart cell survival and demonstrates an essential life-saving role.
Researchers found that vitamin K2 can restore energy production in defective mitochondria, similar to those found in Parkinson's patients. This discovery offers potential treatment options for patients with the disease.
Researchers at Penn have identified a critical role of Nmnat in maintaining healthy nerves and protecting against degeneration. The enzyme helps stabilize mitochondria, which are essential for nerve cell health.
Researchers found that a defect in energy production in the nervous system may be the cause of Parkinson's disease, particularly in younger adults. The study used fruit fly models to discover that a key protein, parkin, is linked to mitochondrial failure and oxidative stress.
A devastating 'founder effect' genetic disorder has been identified as causing defects in mitochondrial energy production in cerebellar neurons. This leads to the development of a debilitating neurodegenerative disease characterized by progressive damage and coordination problems, ultimately resulting in significant disability.
Researchers discovered that genetic mutations causing hereditary Parkinson's disease cause mitochondria to run amok inside cells. Damaged mitochondria produce toxic compounds and fuse with healthy ones, leading to neuronal death.
Researchers have discovered a new genetic defect linked to Leigh syndrome, a devastating mitochondrial disease. The finding offers promise for improved diagnosis and potential treatments.
McMaster researchers discovered that mice without essential exercise genes have impaired muscle function and lower mitochondrial levels. The study highlights the importance of AMPK enzyme in exercise regulation and its potential implications for individuals with mobility issues or obesity.
Researchers at Joslin Diabetes Center have identified the Sirt3 enzyme as a potential target for treating type 2 diabetes and prediabetes. The study found that Sirt3 levels are decreased in skeletal muscle cells of individuals with diabetes, contributing to insulin resistance and energy metabolism issues.
Researchers discovered that mitochondria share a common ancestral lineage with SAR11, a dominant group of marine bacteria. The study provides evidence for the symbiotic origins of mitochondria and sheds light on the metabolic potential of these abundant microorganisms.
Researchers have identified a set of genes within mitochondria crucial to understanding male infertility. Mutations in these genes can build up unnoticed and cause harm to males but not females due to maternal inheritance.
A new study suggests that disrupting the supply chain of nerve cells may contribute to Parkinson's disease. Researchers found that a drug called MPP+ damages mitochondria, which can't be transported to axons, leading to cell death.
Scientists discovered that mitochondria, cell energy factories, produce reactive oxygen species (ROS) causing uncontrolled inflammation in TRAPS. Blocking ROS may reduce inflammation in this disorder and possibly other inflammatory diseases.
Researchers at NIST have developed a technique to extract individual mitochondria from cells, enabling further study of genetic mutations behind neuromuscular disorders. This breakthrough could lead to a better understanding of mitochondrial-based diseases and potential treatments.
Scientists have developed a new class of biofuel cells that can produce electricity using sugar or cooking oil, opening possibilities for recharging portable electronics. The first mitochondria fuel cell successfully produces electricity in lab tests.
Researchers at U of Alberta have found a potential treatment for pulmonary hypertension by targeting the mitochondria in lung blood vessel cells. They discovered that dichloroacetate and trimetazidine can increase mitochondrial activity, inducing cell death and regressing the disease in animal models.
University of Pennsylvania researchers describe a novel mechanism involving calcium transfer between cell components to regulate cell energy. Without this transfer, cells undergo autophagy, or self-eating, as they struggle to produce enough ATP.
Mutations in Parkin cause Parkinson's disease by preventing the clearance of defective mitochondria. Cells expressing mutant Parkin fail to clear damaged mitochondria through mitophagy, a specialized autophagic pathway. This leads to the accumulation of toxic protein aggregates and neurodegeneration.
A team of scientists at UC San Diego identified a protein called Sestrin as a natural inhibitor of aging and age-related pathologies in fruit flies. Sestrin regulates the AMP-dependent protein kinase (AMPK) and Target of Rapamycin (TOR) signaling pathway, which controls aging and metabolism.
Researchers found bacteria developed into complex cells earlier than thought, with mitochondria evolving around 2000 million years ago. The discovery transforms our understanding of cell evolution and the emergence of more complex life forms.
MIT chemists develop a new platinum compound called mitaplatin that selectively destroys tumor cells while leaving normal cells intact. The compound combines cisplatin and dichloroacetate to target cancer cells' altered mitochondrial properties.
A PLoS ONE study suggests that hydrogen peroxide, produced by mitochondria as a by-product of oxygen combustion, may act as a signal molecule regulating daily rhythms and behavior. The research found dramatic effects on fruit fly activity levels and daily rhythms when exposed to hydrogen peroxide.
Scientists have developed a revolutionary technology to analyze protein mixtures, revealing a key enzyme that stabilizes proteins in mitochondria. This breakthrough has significant implications for fundamental research on proteins and their roles in cell function.
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.
OHSU researchers develop gene therapy to prevent inherited diseases such as cancer, diabetes, and neurodegenerative diseases by transferring healthy mitochondria into eggs. The breakthrough could help break the chain of maternally-based diseases passed from generation to generation.
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.