Articles tagged with Mitochondria
A team from the University of Tsukuba has developed a mouse model carrying a disease-associated mitochondrial mutation, which reveals that faulty RNA processing is responsible for metabolic disorders. The study provides new avenues for scientific discovery in understanding mitochondria and multiple diseases.
A study at MedUni Vienna identified a glycerol-3-phosphate shuttle system as an essential back-up in neurons, ensuring sufficient energy supply even when one regulatory system fails. The system follows a hierarchy, with deployment triggered by the failure of other two mechanisms to function adequately.
Research finds that a single dose of alcohol permanently changes brain structure and function, leading to increased risk of addiction. The study used fruit flies and mice models to show that ethanol-induced changes in mitochondrial dynamics and synapse balance contribute to long-lasting behavioral changes.
Researchers found that astrocytes can transfer their mitochondria to damaged neurons after a brain hemorrhage, stimulating the production of an enzyme that neutralizes free radicals. This treatment showed improved neurological recovery in mice, but not if the mitochondria were without the protective enzyme Mn-SOD.
Researchers at Washington University in St. Louis found that cancer cells metabolize glucose in their mitochondria, following conventional biochemical patterns. The study suggests that limiting glucose uptake may not be an effective strategy to target cancer cells, and glucose metabolism may need to be reevaluated as a therapeutic target.
A new study suggests that exercise training is crucial for individuals with diet-resistant obesity, improving skeletal muscle metabolism and enhancing weight loss capacity. The research challenges the one-size-fits-all approach to treating obesity and has the potential to help reshape the science of weight-loss programs.
The workshop will discuss recent advances, perspectives, and applications of medical cannabis and cannabinoids. Researchers will explore their chemistry, pharmacology, analysis, influence on mitochondria, and potential use as anticancer agents.
Research reveals that physical activity has a noticeable effect on almost all brain regions, with higher intensity and duration increasing brain volume and cortical thickness. The hippocampus, a key memory center, benefits most from physical activity, which can help counteract age-related loss of brain matter.
Researchers discovered that human egg cells skip a crucial metabolic reaction to maintain their reproductive capacity without losing energy, allowing them to remain dormant in ovaries for up to 50 years. This finding explains why some women with mitochondrial conditions linked to this reaction do not experience reduced fertility.
The 15th World Congress on Polyphenols Applications will be held in Valencia, Spain from September 28-30, featuring over 100 communications and discussions on polyphenol applications and innovations. The congress aims to explore the role of polyphenols in food and their impact on human health.
Researchers have discovered eight potential leukemia-killing compounds that target mitochondria, inducing mitophagy to weaken cancer cells. The compounds showed significant synergy with existing chemotherapy drugs, offering a deadly one-two punch against leukemia.
A new study from Karolinska Institutet has identified a key mechanism behind treatment resistance in a deadly form of kidney cancer. By increasing mitochondrial content in cancer cells, researchers found that these cells became susceptible to the cancer drug sorafenib. This breakthrough offers hope for more targeted cancer treatments.
Scientists at Karolinska Institutet and Stockholm University have visualized the machinery that mitochondria use to form their proteins. This discovery presents opportunities to design more specific antibiotics and cancer drugs.
Researchers discovered that dermal contact with nicotine concentrations found in thirdhand smoke and electronic cigarette spills can impair wound healing, increase susceptibility to skin infections, and cause oxidative stress in skin cells. The study suggests that even a short exposure of 24 hours is sufficient to cause skin damage.
Researchers investigated the effects of treatment with exogenous Humanin G on inflammation markers in AMD and normal retinal cells. The study found reduced levels of inflammatory proteins in AMD plasma and treated cybrids, highlighting the positive effects of Humanin G.
Eukaryotes emerged in an anoxic environment in the ocean, and their mitochondria-bearing cells likely resulted from a merger between archaea and bacteria. This finding contradicts the long-held view that oxygenation of Earth's surface environment led to eukaryogenesis.
Scientists have successfully developed a gene-editing platform called TALED that can perform A-to-G base conversion in mitochondria, the final missing piece of the puzzle in gene-editing technology. This breakthrough has significant implications for treating previously incurable genetic diseases caused by mutations in mitochondrial DNA.
Researchers discovered that Viagra and a common over-the-counter drug TUDCA restored mitochondrial processes, which drive heart failure in HLHS patients. This could lead to new therapies for treating heart failure without relying on heart transplants.
A study published in the Journal of Cachexia, Sarcopenia and Muscle found that BAM15 improves health outcomes for aged mice with obesity by preventing muscle loss and increasing energy expenditure. The compound helped mice lose fat, gain strength and increase physical activity.
Scientists are working on understanding the interplay between flaviviruses and mitochondria in hopes of finding new treatment options. By deciphering this process, researchers may be able to find broad-spectrum therapeutic targets for diseases like Zika, dengue, and West Nile.
A study suggests that the powerhouse-pruning protein Drp1 plays a crucial role in generating energy for new blood vessel growth, particularly under low oxygen conditions. When oxygen levels are low, Drp1 gets modified to produce reactive oxygen species (ROS), which enables glycolysis and subsequent cell signaling.
Researchers have identified two glucose transporters that disrupt the energy supply to invading worm cells and stop them in their tracks. By deactivating these genes, glucose and ATP levels dropped, and worm cells stalled their spread. This discovery could lead to new ways to cut off cancer cells' fuel lines and prevent metastasis.
Researchers at Massachusetts General Hospital discovered that non-dividing colon cancer cells employ Warburg glycolysis to reduce toxic reactive oxygen species accumulation. This adaptation challenges the long-held dogma of the Warburg effect, highlighting the need for single-cell level analysis tools.
Researchers from Osaka University discovered that MondoA protein delays cellular senescence by activating autophagy, promoting longevity. Activation of MondoA also maintains mitochondrial stability, preventing senescence in tissues like the kidney.
Researchers at University of Cincinnati develop a new probe and imaging technique to study lysosomes, aiding in cancer and neurodegenerative disease research. The probe, known as EC Green, enables multidimensional analysis of lysosome dynamics and provides stable tracking capabilities.
A study published in Science Immunology reveals that a specific neurotransmitter in immune cells plays a crucial role in cholesterol accumulation and sterile inflammation in atherosclerosis. The researchers found that blocking this neurotransmitter may help reduce inflammation and develop effective treatments for the disease.
Researchers at Uppsala University discovered that the ancestors of Legionella bacteria infected eukaryotic cells around 2 billion years ago. This finding challenges the chicken-or-egg debate about which came first, phagocytosis or mitochondria evolution.
Researchers discovered that deficient mitophagy leads to human disease and developed a method to analyze mitochondrial recycling in diseased muscle. Pharmacological activation of mitophagy reversed the progression of mitochondrial muscle disease, offering potential treatment for this condition.
New research from RCSI shows that an irregular body clock can drive inflammation in the body's immune cells, leading to chronic diseases like heart disease and diabetes. Macrophages without a body clock take up more glucose and produce inflammatory products.
Researchers at Brigham and Women's Hospital discovered that cancer cells can disarmed the immune system by forming nanotubes that pull out mitochondria from immune cells. This new mechanism gives a target to go after, leading to potential new combinations of therapies for improving cancer immunotherapy outcomes.
Researchers at Virginia Tech explore mitochondrial differences in CA2 neurons, which encode social memories in the hippocampus. They found unique mitochondrial characteristics in individual neurons, influencing plasticity and behavior.
A team of international scientists has shown that skeletal muscle cells from people with type 2 diabetes have a different circadian rhythm, leading to altered mitochondrial metabolism. The study suggests that considering cellular rhythms when prescribing treatments for type 2 diabetes could optimize their effectiveness.
Researchers found that optimizing energy metabolism through autophagy can improve the immune system response in HIV-affected cells, providing a potential therapeutic approach. This metabolic optimization enables CD4 lymphocytes to better defend against HIV-1 by secreting IL-21, a key protein in defense against the virus.
Researchers at Kyoto University designed a synthetic molecular code, EnPGC-1, that activates mitochondrial biogenesis in T cells, increasing their numbers and longevity. The approach enhances anti-tumor immunity in mice and improves survival.
Researchers reverse lung fibrosis in a mouse model using Bcl-2 inhibitor ABT-199, suggesting a novel therapeutic target to treat idiopathic pulmonary fibrosis. The study finds that monocyte-derived macrophages play a key role in fibrosis progression and that targeting the Cpt1a-Bcl-2 interaction modulates apoptosis resistance.
A new study reveals that the small protein MOTS-c prevents the destruction of insulin-producing pancreatic cells in mice with autoimmune diabetes. MOTS-c treatment supports regulatory T-cells and reduces the activation of killer T-cells, effectively preventing disease onset.
Scientists discovered a new mitochondrial recycling pathway that may help prevent Parkinson's disease. The study, published in Science Advances, reveals that genes associated with Parkinson's disease play key roles in this process and that disruptions can contribute to neurodegeneration.
A study in mice shows that an experimental small molecule helped restore the removal of damaged mitochondria from dopamine-producing brain cells, which may help explain what goes wrong in people with mutations that cause Parkinson's disease. The findings highlight the potential benefit of LRRK2 inhibitors as treatments for the disease.
Researchers at Columbia University Irving Medical Center found a link between psychological stress and graying hair. The study, published in eLife, revealed that hair color can be restored when stress is eliminated. Stress-induced changes in mitochondria may explain how stress turns hair gray.
Researchers found that a shortage of DNA building blocks triggers an inflammatory response in cells when mitochondria release their genetic material. This link could lead to new treatments for various diseases associated with the mitochondrial genome and ageing process.
Scientists discovered SLC25A51 as a key regulator of NAD transport into the mitochondria, a process linked to various physiological and pathological processes. The study opens possibilities for new metabolic therapies against ageing and cancer.
A recent study published in eLife reveals that cheater mitochondria can thrive in simple worms by exploiting cellular stress coping mechanisms. This finding sheds light on the evolution of cheating and cooperative behaviors within organisms, suggesting that competing selection pressures may promote group-level tolerance to cheating.
Researchers have reconstructed a ciliate mitoribosome using cryo-EM, identifying nine novel proteins encoded in the mitochondrial genome and challenging existing views on mitochondrial translation evolution. The discovery provides new insights into mitochondria's structural and functional complexity.
A study using mouse models of Alzheimer's disease found that high calcium levels in mitochondria are associated with plaque deposition and neuronal death. Researchers propose targeting calcium entry to the mitochondria as a promising new therapeutic approach.
Researchers at Penn State have directly observed functional metabolons involved in generating purines, the most abundant cellular metabolites. The findings suggest that enzymes are not haphazardly located throughout cells but instead occur in discrete clusters, or metabolons, that carry out specific metabolic pathways.
Researchers discovered a rescue route that enables cells to repair damage to complex I in mitochondria, a highly sensitive component. This self-help mechanism is more energy-efficient than rebuilding the entire complex and acts as a safety valve to prevent harmful reactive oxygen species.
UCI researchers successfully transplanted healthy mitochondria into cardiomyocytes, boosting cellular energy and improving bioenergetics indices. The study's findings suggest a potential method to mitigate cardiovascular, metabolic, and neurodegenerative disorders.
A new study suggests that increasing energy supply within injured spinal cord nerves could promote axon regrowth and restore motor functions. Researchers found that enhancing mitochondrial transport helped remove damaged mitochondria from injured axons, replenishing undamaged ones to rescue the energy crisis.
Researchers at INSERM have revealed that whole functioning extracellular mitochondria are present in the bloodstream, contradicting previous assumptions. The discovery has significant implications for our understanding of physiology and could lead to improvements in diagnosis and treatment of diseases.
Researchers discovered a phenomenon in brain cells where mitochondria 'eat themselves up' at an early stage of neurodegeneration. The study found that this self-destruction is selectively present in neurons prone to degeneration in ALS patients, providing potential targets for new therapies.
Researchers at Northwestern University have discovered a new phenomenon in the brain where mitochondria self-destruct, leading to early stages of neurodegeneration. The study found that this process occurs selectively in neurons vulnerable to future degeneration, providing a potential target for drug therapies.
Researchers found that natural compounds isolated from Nectandra leucantha can kill parasites causing these neglected diseases. The neolignans displayed bioactivity against Leishmania and Trypanosoma cruzi parasites, which affect millions of people in Brazil and other developing countries.
Researchers at Cold Spring Harbor Laboratory discovered that pancreatic cancer cells destroy their own mitochondria to reduce reactive oxygen species and proliferate. Inhibiting the NIX pathway may prevent cancer cells from using energy to proliferate, offering a promising new target for therapies.
Parkin's activity depends on recruitment and activation by proteins such as PINK1 and MITOL. The discovery of MITOL's role in tagging damaged mitochondria could lead to improved therapies for Parkinson's disease.
A £1.8m funding boost will help researchers at the University of Edinburgh improve diagnosis and treatment outcomes for Crohn's disease, a condition affecting 120,000 people in the UK. The study aims to develop a non-invasive test using blood or stool to determine if the inflamed bowel wall has healed after treatment.
A new microscopy technique, PD imaging, helps isolate highly potent stem cells by measuring mitochondrial activity, potentially improving regenerative medicine outcomes. The method is non-invasive and cost-effective, offering a reliable tool for early-stage stem cell selection.
A high-fat, high-sugar diet in pregnant mice causes heart problems in their offspring, which are then passed down to subsequent generations. The defects in heart mitochondria are thought to be caused by epigenetic changes in the mother's eggs.
A new study suggests that deep brain stimulation boosts the number and strength of mitochondria in brain cells, which may help reduce Parkinson's symptoms. The treatment, used for late-stage Parkinson's disease, involves surgically implanting thin wires into the brain to deliver small electric pulses.
Scientists create a yeast mutant with deficient mitochondria and an E. coli bacterium with the necessary enzymes to form a symbiotic relationship, allowing the chimera to persist for over 40 generations. This model provides insight into the origins of mitochondrial endosymbiosis and can be used to explore further mechanisms.
Researchers at Jefferson University have identified a molecular lock and key that controls calcium's entry into mitochondria, revealing a new target for drug discovery. The finding suggests that compounds like ruthenium red/360 can block calcium entry into cells, potentially treating neurodegenerative diseases.