Articles tagged with Mitochondrial Function
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A new study found that rapamycin impairs mitochondrial function in guinea pig models of osteoarthritis, worsening disease severity. The drug, which extends lifespan, also caused a rise in blood glucose levels and impaired skeletal muscle function.
New research reveals TMEM126A gene mutations cause mitochondrial energy production issues, leading to impaired vision and hearing. Mitochondrial disease affects almost any part of the body due to reduced energy conversion and production.
A mouse study found that vitamin D deficiency impairs skeletal muscle mitochondrial function, leading to reduced energy production and potentially poor muscle strength. The study suggests that preventing vitamin D deficiency in older adults could help maintain better muscle function and reduce age-related muscle deterioration.
Researchers at Kumamoto University found that ketogenesis maintains mitochondrial function, preventing excessive acetylation and fatty liver development. This discovery may lead to future therapies for protecting mitochondria and organs in newborns and individuals with nutritional deficiencies.
Researchers have developed a simple, high-throughput method for transferring isolated mitochondria into mammalian cells, allowing for the study of mitochondrial DNA diseases and potential treatments. The new device, MitoPunch, enables the transfer of mitochondria into thousands of recipient cells simultaneously.
A study identified mitochondrial biomarkers as significant contributors to memory decline after menopause, shedding light on the importance of energy production in women's cognitive health. Researchers found that efficient mitochondrial function was associated with better cognitive performance, particularly in executive functions.
Researchers at CNIC and IIS Princesa discover that sodium ions regulate mitochondrial function, increasing reactive oxygen species production in early stages of hypoxia. This finding could lead to new treatments for diseases related to hypoxia, such as stroke and heart attack.
Researchers discovered abnormalities in communication between brain cells and molecular changes affecting protein production due to dysfunctional CASK gene. The study also suggests an unexpected role for CASK in regulating energy production in cells, which may explain diminished brain size and dysregulated function.
Researchers at Karolinska Institutet have discovered that a lack of mitochondria causes severe disease in children, including brain dysfunction and neurological impairment. The study, published in EMBO Molecular Medicine, suggests that inhibition of mitochondrial degradation may provide a new treatment strategy for affected patients.
Research at Max Planck Institute for Biology of Ageing reveals that NFYB-1 regulates mitochondrial function through lysosomal prosaposin, a key factor in cellular longevity. The study used Caenorhabditis elegans as a model organism and found that restoring cardiolipins improved worm health.
A newly-discovered small protein in mitochondria is essential for energy production, according to a study by Duke-NUS Medical School. The protein, named BRAWNIN, was found to be necessary for the assembly of a critical molecular complex involved in oxygen-based energy generation.
Researchers have developed a new tool to study how mitochondrial protein synthesis is affected by disease, pharmaceuticals, ageing and different physiological situations. The MitoRibo-Tag mice provide a valuable tool for future studies on how mitochondrial function regulates human health.
Cambridge researchers have discovered that placentas can adapt to function properly despite poor diets or low oxygen during pregnancy, impacting on pregnancy outcomes and lifelong health. This adaptation helps the placenta transport sufficient oxygen and nutrients to the fetus, mitigating complications such as fetal growth restriction.
Scientists at Scripps Research have discovered how neurons manage mitochondrial transport, a process crucial for nerve cell function and energy production. The study found that cAMP signaling enhances mitochondrial transport after synapse formation, requiring significant energy to maintain communication between cells.
A study by Mohammad Asghar seeks to understand age-related kidney function impairment and identify targets for drug interventions. The researcher believes that mitochondrial respiration plays a critical role in maintaining normal kidney function.
Researchers found that papaverine reduces tumor oxygen consumption and hypoxia in mouse models, making tumors more sensitive to radiation. This suggests repurposing papaverine to enhance radiation therapy effectiveness.
A new study found that long-term heat therapy increases mitochondrial function in the muscles by an average of 28 percent. Heat therapy may provide a new treatment option for people with chronic illness or disease who cannot exercise regularly.
A recent study published in Science Signaling reveals that the ATM protein plays a dual role in sensing cellular threats and repairing damage. It forms dimers when exposed to ROS, triggering an increase in cellular antioxidant capacity through the pentose phosphate pathway.
A genetic mutation in the MPP gene can lead to impaired functioning of proteins needed for mitochondrial protein import, resulting in accumulation of immature proteins and interference with mitochondrial functions. This study identified the molecular consequences of this mutation, providing a fundamental explanation for the disease.
Scientists at Northwestern University discovered that mitochondria and lysosomes directly contact each other in cells to regulate their functions. This rare finding has important implications for understanding normal aging and diseases such as Parkinson's and cancer.
Researchers have identified EXD2 as a critical regulator of mitochondrial protein production, which is essential for energy generation and maintaining cellular homeostasis. The study found that EXD2 targets messenger RNA to facilitate the maturation of the mitochondrial ribosome, leading to increased protein production.
A new study from the University of Bergen shows that impairment in mitochondria may actually protect the brain in Parkinson's disease. Brain cells with decreased complex I levels are less likely to contain Lewy bodies, abnormal protein-aggregates that characterize Parkinson's disease.
Researchers found that maternal e-cigarette vaping increases the risk and severity of allergic asthma in offspring, with detrimental effects partially mediated through mitochondrial function. The study highlights the need for caution when considering e-cigarettes as a safe alternative to cigarette smoking during pregnancy.
A new study finds that quaternary ammonium compounds (quats) inhibit mitochondria, the powerhouses of cells, and estrogenic functions. This raises concern about their impact on human health and potential reproductive harm.
Scientists from the University of Freiburg successfully mapped the mitochondrial protein landscape, revealing over 200 new proteins not previously attributed to this organelle. This study provides a basis for studying the potential new functions of mitochondria and understanding various diseases.
Researchers at Temple University Health System reveal that mitochondrial calcium efflux is essential for proper heart function and identifies a promising therapeutic target to limit heart disease. The study shows that augmenting NCLX expression can prevent cell death and protect against the progression of heart failure.
Scientists discovered that 'bad' mitochondria accumulate in old kidneys, leading to permanent damage and renal failure. Preliminary training may not be effective in older animals due to impaired quality control mechanisms.
A Mayo Clinic study found that high-intensity aerobic exercise can reverse cellular aspects of aging, improving lean body mass and insulin sensitivity. The study also showed that high-intensity interval training enhanced muscle protein content, causing muscle enlargement and improving energetic functions.
Researchers discovered a link between genes nardilysin and OGDHL, which are crucial for mitochondrial function, and progressive loss of neurological functions in humans. Mutations in these genes lead to neurodegeneration, characterized by the accumulation of cellular trash.
Researchers found that the Parkin gene is turned on in response to environmental insults causing free radical formation and cataract development. Parkin helps prevent free radical damage and increases lens cell survival.
Scientists have created clusters of spherical compartments by mimicking natural organelle structures. The synthetic compartments were connected using DNA bridges, enabling controlled properties and architecture.
Researchers at the CNIC have defined the molecular organization underlying energy production in living cells. The discovery sheds light on the regulation of metabolism and reveals a new understanding of the mitochondrial electron transport chain's structure and function.
A recent study published in Cell Metabolism has discovered that a compound called NAD can reverse muscle degeneration in mice with tissue aging. The research, led by the University of Pennsylvania School of Medicine, found that NAD supplementation improved muscle function and reduced inflammation in aged mice.
Researchers at Amazentis SA and EPFL have discovered that urolithin A boosts mitochondrial function and reverses muscle aging. Oral administration of the compound enhances muscle strength and endurance in aged rodents.
Researchers found that nicotinamide riboside improves mitochondrial function in stem cells, leading to better regeneration processes in aged mice. The compound also showed promising effects on the brain and skin, with potential implications for regenerative medicine.
Georgia State University biologist Ming-Hui Zou has received a four-year, $1.9 million NIH grant to study the role of AMPK in cellular energy balance and its relation to cardiovascular disease. His research aims to unravel the interplay between mitochondrial structure and function in the initiation of cardiovascular disease.
Researchers identify LMIT1, a mitochondrial iron transporter in Leishmania parasites, as crucial for parasite virulence. Inhibiting LMIT1 function can abolish parasite virulence and reduce disease severity.
A recent study by McGill University researchers has found that ubiquinone, a widely believed antioxidant, is unlikely to provide benefits for cell protection. The study used mice with controlled ubiquinone biosynthesis levels and discovered no signs of oxidative damage despite the loss of the substance.
A recent study at Vanderbilt University Medical Center has identified a crucial 'guardian' protein called CHIP that monitors mitochondrial function in the brain. The absence of this protein leads to profound impairments in mice with the CHIP gene deleted, highlighting its critical role in maintaining healthy nerve cells.
Researchers have made significant discoveries about coenzyme Q and its production pathway, shedding light on mitochondrial function and its link to human diseases. Two new studies published in PNAS and Molecular Cell reveal the biochemical functions of key proteins involved in coenzyme Q synthesis.
Researchers at the University of Helsinki found that vitamin B3 form, nicotinamide riboside, can delay the signs of mitochondrial myopathy in animal models. The treatment increased mitochondrial mass and function, curing structural abnormalities and providing a potential therapeutic approach for adult-onset mitochondrial muscle diseases.
Researchers confirm their 2008 model for mitochondrial function, which explains the symptoms of diseases and reveals the role of five molecular machines in converting energy. The study also highlights the dynamic nature of mitochondrial energy extraction, which can be optimized based on dietary composition.
Researchers found that herpes viruses and other neurotropic pathogens sabotage cell function by hijacking neuronal internal transportation networks. Viral infection elevates neuron activity and calcium levels, stopping mitochondrial motion and allowing the virus to freely travel and reproduce within infected cells.
A team of scientists has discovered a new family of six genes that regulate mitochondrial transport in neurons, which is crucial for brain activity and viability. The proteins are highly expressed in the nervous system and may be involved in neurological conditions such as Parkinson's disease and Charcot-Marie-Tooth disease.
New research confirms resveratrol's role in prolonging lifespan and health through SIRT1-activated mitochondrial function. Studies using mouse models show that without SIRT1, resveratrol has no beneficial effect on energy production.
A team of scientists at Karolinska Institutet has identified a key component in mitochondria's function, which combines with another protein to control ribosome formation and energy production. The discovery sheds light on the regulation mechanisms involved in inherited and age-related diseases.
Overexpression of PGC-1α significantly improves neurological function in HD-model transgenic mice by reducing htt protein aggregation and oxidative stress. This discovery may lead to therapies targeting PGC-1α function for treating Huntington's disease and related disorders.
Scientists at IRB Barcelona have identified a new protein crucial for mitochondrial function in the fruit fly Drosophila melanogaster. The removal of this protein leads to aberrant mitochondria and metabolic capacity loss, causing death.
Researchers found that damaged mitochondria in the brain's neurons can lead to impaired synapses, crucial for normal brain function. Modifying cyclosporin, a drug already approved for organ transplant patients, may help slow down Alzheimer's disease at its earliest stages.
A study reveals that mutant SOD1 interacts with VDAC1, disrupting its function and leading to mitochondrial damage and motor neuron degeneration. Reduced VDAC1 activity accelerates the onset of fatal paralysis in ALS mice.
Scientists at EMBL have identified IRPs as key proteins ensuring iron balance in cells. In a study, they found that IRPs are required for mitochondrial function and that their dysfunction leads to iron deficiency and cellular damage.
Researchers at the University of Florida found that anti-aging supplement mixtures may be more effective in preventing decline in physical function than single compounds. Taking such supplements before very old age can lead to improved grip strength and mitochondrial function, suggesting a potential window for intervention.
A low protein diet boosts mitochondrial function, extending lifespan in flies. This discovery has implications for human aging and diseases such as obesity, diabetes, and cancer.
Parkinson-associated genes PINK1 and Parkin functionally interact to maintain mitochondrial function, impairing neuron loss
A recent study published in Science found that the STAT3 protein plays a key role in converting normal cells to cancerous cells by regulating gene expression in both the cell nucleus and mitochondria. This discovery may lead to the development of targeted cancer therapies.
Scientists identified a protein that regulates mitochondrial movement in brain cells, shedding light on how the brain recovers from stroke. Understanding this mechanism may help identify novel approaches for preventing and treating neurological disorders.
Researchers have developed a mouse model of Wolfram Syndrome, linking CISD2 gene function to mitochondrial integrity and aging. CISD2-deficient mice display premature aging, decreased body weight, and degeneration of optic and muscular tissues.
Researchers discovered that PARL plays a key role in initiating apoptosis in mitochondria, leading to faster cell death and increased risk of diseases like Parkinson's. The study used 'knock-out' mice that lacked PARL, showing that the protein is essential for protecting cells from controlled cell death.
Researchers found substances increasing mitochondrial size also boost cardiac contractility. This effect isn't related to energy production; instead, it suggests a form of mechanical signaling between organelles in cardiac cells. The study opens possibilities for developing drugs that enhance heart function.
Researchers discover that excessive amyloid-beta toxicity leads to functional heme deficiency, causing mitochondrial decay and oxidative damage. A new class of targeted drugs could soon be developed to address this underlying mechanism.