Articles tagged with Mitochondrial Dysfunction
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Researchers developed a new approach using the microbial protein Archaerhodopsin-3 to induce apoptosis in cancer cells, leading to significant tumor shrinkage when exposed to green light. The findings, published by Okayama University, show great potential for this light-activated molecule as a novel cancer therapy.
Researchers from Trinity College Dublin discovered that nanoplastics can interfere with brain energy production by disrupting the electron transport chain in mitochondria. This finding may have implications for understanding neurodegenerative diseases and learning/memory issues.
Mitochondrial dysfunction is linked to various diseases, including neurodegenerative disorders and cancers. Mitochondria can be transferred between cells via tunneling nanotubes, restoring cellular respiratory function. Understanding mechanotransduction pathways involving mitochondria is essential for developing effective therapies.
Researchers found that diabetes directly affects the heart's structure and energy production in humans for the first time. Diabetes causes distinct molecular changes to heart cells and structural changes to the muscle, particularly in patients with ischaemic cardiomyopathy.
This review synthesizes evidence highlighting immune aging as a critical accelerator of type 2 diabetes pathogenesis. Chronic low-grade inflammation, organelle stress pathways, and the ominous octet framework contribute to metabolic-inflammatory vortex, disrupting β-cell function and insulin signaling.
Long-haul COVID-19 and myalgic encephalomyelitis/chronic fatigue syndrome share similar pathophysiologies, including oxidative stress, autoantibodies, and impaired mitochondrial energy conversion. These conditions also exhibit neurodegenerative outcomes, such as fatigue, sleep disturbances, and increased risk of dementia.
Research discovers mitochondrial respiration impairment accelerates skeletal ageing by altering cell metabolism and reducing regenerative abilities. The study highlights the role of mitochondria in skeletal health and potential therapeutic avenues.
Novel biomarkers like miRNA-34a link anthracyclines to cardiotoxicity, while stem cell therapy and nanotechnology offer potential for prevention and treatment. Traditional strategies have limitations, but new approaches hold hope for improved patient outcomes.
Researchers found that gasdermin D promotes atrial arrhythmogenesis by facilitating the formation of pores in cell membranes and releasing cytokines. A mitochondrial-targeted therapy approach may prevent AF triggering, positioning gasdermin D as a promising therapeutic target.
A study from University of California San Diego reveals a direct association between inherited genetic variants in mitochondrial DNA and the severity of Gulf War illness. The findings support an emerging hypothesis that GWI is driven by mitochondrial dysfunction rather than inflammation.
Researchers identify TRMT10C enzyme causing methylation of ND5 mRNA, leading to mitochondrial dysfunction and reduced energy supply to the brain. Impairment of complex I in the respiratory chain contributes to Alzheimer's disease pathology.
Long-term treatment with methylene blue (MB) and mitoquinone (MitoQ) did not alter age-related bone loss in mice. Antioxidant interventions are insufficient to inhibit skeletal aging, suggesting alternative approaches may be needed.
A study by researchers from Japan has revealed that cysteine persulfide, produced by cysteinyl-tRNA synthetase, regulates cellular longevity in budding yeast. The study found that introducing supersulfides can reverse detrimental effects on mitochondrial energy metabolism and protein quality.
A study published in PNAS reveals that HKDC1 protein plays a crucial role in maintaining mitochondrial and lysosomal function, thereby preventing cellular senescence. The researchers found that HKDC1 helps regulate the removal of damaged mitochondria through mitophagy and facilitates lysosomal repair.
Researchers identified a novel bacterial protein, MceF, that can prolong cell longevity by acting directly on mitochondria. The discovery could lead to new treatments for diseases relating to mitochondrial dysfunction, such as cancer and auto-immune disorders.
Researchers created an immunodeficient mouse model of physiological ovarian aging, mirroring female fertility decline with age. The study found decreased oocyte quality, impaired follicle activation and growth, and increased mitochondrial dysfunctions in Old mice.
Researchers found that SARS-CoV-2 alters mitochondria on a genetic level, leading to widespread 'energy outages' throughout the body and its major organs. This affects the heart, brain, and lungs, contributing to long COVID symptoms.
A study published in Neurobiology of Disease suggests that targeting the sigma-1 receptor and ATAD3A protein may prevent mitochondrial dysfunction in ALS. The researchers found that this approach could lead to a novel therapeutic strategy for neurodegenerative diseases.
A recent study found that the mitochondrial antioxidant MitoQ can reverse the detrimental effects of HIV and antiretroviral therapy on organs such as the brain, heart, and liver. The researchers used humanized mice infected with HIV and treated them with MitoQ for three months.
Researchers create advanced imaging-based method for studying mitochondria, enabling detailed mapping and measurement of structural changes. This technique has potential applications in understanding diseases such as Alzheimer’s, Parkinson’s, and cancers where mitochondrial function is disrupted.
Nicotinamide riboside has been found to increase muscle mitochondria, improve gut bacterial composition, and boost NAD+ concentrations in humans. The findings suggest that NR supplementation may be a promising therapeutic option for diseases characterized by muscle mitochondrial dysfunction and/or gut microbiota imbalance.
Researchers discover gene therapy ophNdi1 that boosts mitochondrial performance in retinal ganglion cells, potentially treating glaucoma and age-related macular degeneration. The therapy shows protective effects in three models of mitochondrial dysfunction.
Researchers from Osaka University have identified a system known as the GET pathway as crucial for regulating the numbers of energy-producing mitochondria. The study found that disruption of the GET pathway leads to reduced mitophagy, a process responsible for removing defective or excess mitochondria.
A study published in Aging-US reveals changes in gene expression associated with age-related muscle loss and frailty. Researchers identified unique cellular subpopulations in aged and sarcopenic skeletal muscle, which may facilitate the development of new treatments for age-related frailty.
Researchers identified a genetic variant linked to digestive disturbances in patients with Chagas megaesophagus, a disorder characterized by esophageal dilation and loss of motility. The study suggests that increased interferon-gamma production leads to mitochondrial dysfunction, contributing to the development of the disease.
ATAD3A is crucial for the movement of genetic material inside mitochondria, affecting energy production. The correct distribution of mtDNA nucleoids activates expression of respiratory chain complexes.
Researchers from Hokkaido University have identified a link between succinyl-CoA levels and energy metabolism in heart cells affected by chronic heart failure. Supplementation with 5-aminolevulinate acid improved heart function and oxidative phosphorylation capacity in mice with surgically blocked blood supply.
Scientists at Duke-NUS Medical School have discovered the critical role of small microproteins in assembling larger protein complexes inside energy-generating cell components known as mitochondria. The study highlights how microproteins regulate energy supply and mitigate mitochondrial dysfunction, a feature underlying various diseases.
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 randomized clinical trial found that GlyNAC supplementation improves age-associated defects in older humans, including oxidative stress and mitochondrial dysfunction. This led to improvements in muscle strength, gait speed, exercise capacity, and other health outcomes, showing promise for promoting healthy aging.
Researchers developed a non-invasive ocular imaging method to detect flavoprotein fluorescence in the eye, indicating mitochondrial oxidative stress. This technique may predict glaucoma progression earlier than current methods, with similar sensitivity to visual field changes.
Researchers discovered that a conserved receptor molecule called Tom70 coordinates the balance between protein production and import into mitochondria. This finding ties to increased lifespan and delayed mitochondrial dysfunction when Tom70 levels are elevated. The study provides new insights into aging and age-related diseases.
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.
Scientists demonstrate a definitive link between mitochondrial oxidative damage and cognitive dysfunction in Alzheimer's disease using a transgenic mouse model. The study found that Aβ1-42 aggregation in the hippocampus caused cognitive impairment, while oxidation led to mitochondrial dysfunction.
A new pathway has been discovered to explain how excessive alcohol consumption damages the liver, specifically through mitochondrial dysfunction. By targeting an enzyme called MATα1, researchers believe they can develop a new treatment for people suffering from alcohol-associated liver disease.
Researchers at Goethe University and the Max Planck Institute of Biophysics have gained new insights into how mitochondrial complex I facilitates proton transfer through water molecules. The study's high-resolution structure data enabled computer simulations that shed light on the protein's dynamics during its catalytic cycle.
A team of University of California, Irvine scientists discovered a novel pharmacological approach to attenuate mitochondrial dysfunction that drives diet-induced obesity. They found that a small molecule, SH-BC-893, can correct metabolic disease even when mice continue to consume an unhealthy Western diet.
Scientists from Trinity College Dublin have developed a new gene therapy approach that successfully protected the visual function of mice with dysfunctional mitochondria. The treatment also improved mitochondrial performance in human cells with OPA1 gene mutations, offering hope for treating diseases like Alzheimer's and Parkinson's.
A study found mitochondrial dysfunction to be a common thread driving damage in astronauts' bodies during extended space travel. Researchers used data from various sources and identified alterations affecting biological function as the key issue.
Researchers discovered a metabolic adaptation in nerve cells that allows them to counteract degeneration and promote survival. This 'metabolic rewiring' involves the activation of the Krebs cycle anaplerosis pathway, which makes neurons resistant to progressive damage.
Researchers at the Medical University of South Carolina have developed a vitamin K-based compound that eliminates medication-resistant epileptic seizures in mice. The compound works by increasing brain cells' ability to produce energy and protects mitochondrial health, making it a promising new treatment option for those with epilepsy.
Researchers at RIKEN Center for Brain Science found mitochondrial dysfunction affects serotonergic neurons in mice with ANT1 mutations, linking the two pathways.
A study of mitochondrial DNA found higher levels of lesions and extra copies of genes in veterans with Gulf War illness, suggesting excess DNA damage. This supports the idea that mitochondrial dysfunction contributes to symptoms and persistence of GWI.
Aging cells of progeria patients can be recovered by inhibiting ROCK protein activation and increasing mitochondrial function through the use of drug Y-27632. This study identifies a molecular causal relationship between mitochondrial dysfunction and cell senescence, offering new hope for treating premature aging syndromes.
Researchers used genetically-modified mice to study hereditary deafness caused by mitochondrial dysfunction. Reducing enzyme activity in mice showed promise for preventing or delaying deafness, according to new research.
Researchers at Temple University School of Medicine have identified a protein that opens the door to cell death, causing severe power failures in mitochondria. Blocking this protein with a small molecule inhibitor could aid in the treatment of cardiovascular diseases such as heart attack and stroke.
Researchers have found a potential target for treating mitochondrial disorders, a condition that affects cellular energy production. The study suggests that blocking the gene ATPIF1 may be therapeutic in rescuing cells from mitochondrial dysfunction.
A UC Davis study found that children with autism have more trouble fueling their cells due to dysfunctional mitochondria. The researchers analyzed blood samples from 10 children with autism and 10 typically developing children, detecting mitochondrial dysfunction and changes in mitochondrial DNA.
Researchers discovered that children with full syndrome autism have impaired mitochondrial function and mitochondrial DNA abnormalities, which may contribute to brain dysfunction. The study suggests that mitochondrial dysfunction could amplify and propagate brain problems in autism.
A new study by UC Davis researchers found that children with autism have deficits in cellular energy production, suggesting a strong link between autism and mitochondrial defects. The study's lead author suggests that deficiencies in mitochondria may contribute to cognitive impairments associated with autism.
Atrial tachycardia is associated with mitochondrial dysfunction and oxidative stress, leading to NF-kB activation. Blockade of angiotensin II receptors, L-type calcium channels, NADPH oxidase, and inhibition of NF-κB activation can abolish or decrease tachycardia-dependent changes in atrial tissue.