A new Northwestern Medicine study reveals how metformin lowers glucose levels by targeting mitochondrial complex I in cells. The drug also improves COVID outcomes and reduces inflammation, suggesting that mitochondrial complex I inhibition may be a unifying mechanism behind its diverse effects.
A new study shows targeted delivery of energy-disrupting gene therapy using nanoparticles shrinks glioblastoma brain tumors and aggressive breast cancer tumors in mice. The technology, mLumiOpto, induces light-activated electrical currents inside cells to disrupt mitochondria, leading to programmed cell death and DNA damage.
Low-cost sequencing technology has opened a flood of mitochondrial DNA data on lice and other insects, bolstering studies on insect species identification and developing insecticides. This genetic data also offers insights into the impact of evolution on neurodegenerative diseases and potential pest control methods.
Researchers found peculiar mitochondria-like symbionts in freshwater lakes, groundwater, and wastewater worldwide, revealing surprising metabolic capacities. They can respire oxygen in addition to nitrogen, impacting the nitrogen cycle and potentially producing greenhouse gases.
The AAAS Annual Meeting will take place in-person in Boston from February 13-15. The event features a range of press events, including a Science Trends Media Briefing and a Press Lunch with Experts, offering opportunities for journalists to engage with science professionals and stay up-to-date on the latest news and trends.
Mitochondria regulate cell death and inflammation by releasing pro-inflammatory messenger substances, a process controlled by the NLRP3 sensor. This discovery could lead to new treatments for inflammatory diseases such as gout, type 2 diabetes, and severe COVID-19.
A new award at University of Utah Health recognizes the importance of a diverse scientific community. The Administrative Supplement to Recognize Excellence in Diversity, Equity, Inclusion, and Accessibility (DEIA) Mentorship award aims to enhance diversity, equity, inclusion, and accessibility in biomedical sciences.
Dr. Andreazza's work focuses on identifying biomarkers for personalized treatments in metabolic psychiatry, with breakthroughs in brain organoids and mitochondrial transplantation techniques. Her innovative approach aims to revolutionize treatment for both psychiatric and metabolic disorders.
Researchers at USC Dornsife discover that mifepristone increases mitophagy to the same extent as rapamycin, potentially extending lifespan. The study found that combining the two drugs does not offer additional benefits and slightly reduces lifespan, suggesting they act through the same biological pathway.
Scientists discovered a unique way in which yeast cells adapt to starvation by coating their mitochondria with massive molecular complexes called ribosomes. This adaptation has potential implications for cancer treatment as it may help overcome the challenges faced by cancer cells when they are starved of nutrients.
A group of scientists discovered that the Black and white tegu lizard can raise its own body temperature during the reproductive season, even in a dark burrow. The study found that this phenomenon is due to the increased production of mitochondria and a protein called ANT, which generates heat.
Parents who struggle with alcohol use disorders can pass along symptoms of early aging to their children, affecting them well into adulthood. These accelerated aging effects include high cholesterol, heart problems, arthritis, and early onset dementia.
A study from the University of California, Berkeley, shows that nematodes react to pathogenic bacteria by destroying mitochondria to protect against iron-stealing bacteria. This protective response suggests that humans may also respond to the smell of pathogens to prepare their gut for infection.
A recent study from China has found that Cordyceps sinensis can ameliorate idiopathic pulmonary fibrosis in mice by inhibiting mitochondrion-mediated oxidative stress. The fungus was shown to reduce pulmonary inflammation and collagen deposition, offering a promising alternative for patients suffering from this debilitating disease.
A new technique, METAPHOR, visualizes embryo metabolism to predict implantation success and full-term birth, increasing the probability of success in assisted reproduction processes.
A new study from Columbia University Irving Medical Center suggests that the brain's mitochondria play a fundamental part in translating feelings and experiences into physical changes. Researchers found that older adults with lower psychological stress had greater mitochondrial energy transformation machinery, linked to higher well-being.
Researchers found that mitochondrial GRIM19 loss induces liver fibrosis through NLRP3/IL33 activation via reactive oxygen species/NF-кB signaling. This mechanism may provide potential therapeutic approaches for preventing early-stage liver fibrosis.
A genomic study uncovers germline ARID1B and mitochondrial variants that may drive pediatric chordoma genesis, a rare and aggressive bone tumor. The study found aberrant indels and haywire mitochondria in 22% of pediatric chordoma samples.
A head-mounted device generating an ultra-low frequency magnetic field has improved symptoms of four male patients with major depressive disorder. The study suggests that future trials may offer a safe and non-invasive way to treat depression.
Researchers at Karolinska Institutet have discovered a new class of drugs that block mitochondrial function and reverse diet-induced obesity, fatty liver, and diabetes in mice. The treatment increased fat metabolism, leading to drastic weight loss and restored glucose tolerance.
Researchers at Max Planck Institute discover that liver mitochondria adapt to food presence via nerve cells, leading to improved insulin sensitivity. This finding could pave the way for new type 2 diabetes treatments.
Researchers identify mitochondrial priming as a key driver of multi-drug resistance in relapsed acute myeloid leukemia. A new technique called dynamic BH3 profiling reveals anti-cancer drugs capable of overcoming resistance.
In nerve cells, insulin facilitates the elimination of defective mitochondria when energy is available. However, during energy scarcity or disrupted insulin signaling, mitochondrial recycling is reduced, allowing potentially damaged power plants to continue operating. This process affects ageing processes and neurological diseases.
A study by UNC researchers found that a metabolic enzyme called Acetyl-CoA Carboxylase (ACC) causes T cells to store fat rather than burning it for energy in solid tumors. Inhibiting ACC expression allowed T cells to persist better in tumors, leading to potential breakthroughs in immunotherapies like CAR T-cell therapies.
Cells use autophagy as a recycling system to transport and break down damaged organelles, including mitochondria. A recent study reveals the molecular details of how an enzyme called TBK1 participates in mitophagy, a disease-relevant process linked to Parkinson's disease.
Researchers created novel gene editing enzymes with improved precision, reducing off-target RNA edits by over 99%. The technology has potential applications in treating mitochondrial genetic diseases and may lead to transformative treatments within the next five years.
A recent study by Swansea University analyzed the link between digit ratio and oxygen consumption in professional football players. The research found that athletes with longer ring digits relative to their index fingers had more efficient oxygen metabolism, reaching high maximal oxygen consumption during a cardiopulmonary test.
Researchers developed a high-speed modulation system combining digital display with super-resolution imaging, significantly improving lateral and axial resolution. This enables detailed study of subcellular structures in animal cells and plant ultrastructures, paving the way for future biological discoveries.
Researchers identified mechanisms that cause ponatinib to harm the heart and found a promising treatment that could reverse this process. The treatment protects heart cells without diminishing the tumor-fighting efficacy of the drug.
Scientists discovered a novel mechanism for removing mtDNA from mitochondria, which can initiate an immune response promoting inflammation. The discovery reveals new targets for therapeutics to disrupt the inflammatory pathway and mitigate inflammation during aging and diseases.
Indiana University researchers have found that nicotinamide nucleotide adenylyl transferase 2 (NMNAT2) plays a critical role in protecting the brain from aging and neurodegenerative diseases. The enzyme provides energy to axons, enabling them to carry out nerve impulses and maintain healthy function.
A study published in Nature Metabolism reveals that obesity is associated with the fragmentation of mitochondria in fat cells, leading to reduced energy burning and weight gain. Researchers identified a single gene responsible for this process and found that deleting it protected mice from diet-induced weight gain.
Researchers develop technology that alleviates retinal pathologies by targeting mitochondrial chaperone TRAP1, which is implicated in the breakdown of blood-retinal barrier and pathological neovascularization. This treatment approach holds great promise for revolutionizing the treatment landscape for ischemic retinopathy.
A new task force launched by C-Path aims to accelerate drug development for mitochondrial and inherited metabolic diseases. The task force will leverage C-Path's expertise in data management standards, biomarkers, and regulatory science to generate solutions and contribute to regulatory decision-making.
A team of scientists identified VAP as a molecular anchor that stabilizes mitochondria near synapses in dendrites, supporting memory formation and plasticity. The discovery links VAP to ALS-linked protein and suggests that mitochondrial stabilization is critical for neuronal function and health.
A newly identified genetic mutation in a small protein provides significant protection against Parkinson's disease. The variant, SHLP2, is found primarily in people of European descent and reduces the risk of Parkinson's by twofold.
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.
A new study found that multiple members of the oxymonad lineage have lost their mitochondria, a crucial energy-producing organelle, approximately 100 million years ago. This discovery suggests that it's possible for eukaryotic organisms to thrive without mitochondria, paving the way for further research on their evolution and adaptations.
Researchers found that genetic variations in the Eif4enif1 gene lead to premature ovarian insufficiency and reduced egg production. The study suggests that restoring proper mitochondrial behavior could improve fertility in human patients with similar conditions.
Researchers discovered that Osteopontin induces mitochondrial biogenesis in deadherent breast tumor cells, which aids metastatic success. The study suggests a possible mechanism and targets for treating cancer metastasis by increasing ATP levels and mitochondrial mass.
A recent study found that transient inflammatory pain causes persistent mitochondrial and metabolic disturbances in sensory neurons, leading to failure in pain resolution. Targeting the cellular redox balance prevents and treats chronic inflammatory pain in rodents.
Dr. Vidhya Rangaraju has received a $1.2 million grant from the Chan Zuckerberg Initiative to investigate disrupted energy supply in neurons causing cognitive decline in ALS. Her lab will use super-resolution microscopy and biosensors to study metabolic disruptions in ALS.
Researchers identify protein SLC25A39 as a double-functioned nutrient sensor and transporter for mitochondria, regulating glutathione levels to prevent oxidative stress. The discovery sheds light on the critical role of glutathione in maintaining mitochondrial function.
Researchers developed a drug that triggers the destruction of damaged mitochondria, restored motor function in aging mice with ALS-like symptoms. The results show promising promise for treating neurodegenerative diseases like Parkinson's and Alzheimer's disease.
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.
Researchers developed three new two-photon probes that can visualize organelles in cells, enabling better understanding of cellular functions and tissue imaging. The probes are designed to detect pH levels, viscosity, and ionic species, providing more specific insights into cell viability and treatment responses.
Researchers discovered that fine-tuning mitochondrial energy production reduces melanoma tumor growth and enhances immune response in mice. The study reveals that manipulating mitochondrial electron transport increases expression of immune genes and makes tumor cells more visible to killer T cells.
Researchers found that mature sperm carry only 100 organelles with mitochondria but no intact mtDNA. This discovery has important implications for human fertility and germ cell therapy, potentially limiting the risk of accumulating harmful mtDNA mutations.
A new Northwestern Medicine study reveals that a dysfunction in the neuron's synapses leads to deficits in dopamine and precedes neurodegeneration in Parkinson's disease. The findings suggest targeting dysfunctional synapses before neurons degenerate may represent a better therapeutic strategy.
A novel mitochondrial enzyme was identified as key to reproductive aging, increasing oocyte clustering with age and affecting fertility
Researchers have found that the protein Musashi-2 plays a crucial role in regulating type 2a muscle fiber mass and metabolism. The study reveals that Msi2 knockout mice exhibit reduced muscle mass, decreased myoglobin and mitochondria levels, and impaired sugar metabolism.
Researchers discover compound Urolithin A restores mitochondrial function in hematopoietic stem cells, rejuvenating blood reconstitution capability and improving immune system function. The study shows promising results in aging mice, paving the way for potential interventions targeting age-related health conditions.
Researchers have found that mouse stem cells mimic their parent animals' cold resistance, generating energy differently at low temperatures. This discovery opens up new avenues for studying organ preservation and human hibernation using in vitro models.
Researchers at West Virginia University are tracing the cause of diabetic heart disease using diabetic animal models to examine mitochondrial function. They hope to understand how faulty protein import affects the mitochondria and explore potential treatments to improve energy production and reduce cardiovascular risk.
A study by Children's Hospital of Philadelphia found that COVID-19 affects mitochondrial function in multiple organs beyond the lungs, leading to long-term damage. Mitochondrial gene expression was suppressed in the heart, kidneys, and liver, while recovering in the lungs.
Researchers at the University of Virginia Health System discovered that improper calcium signaling in mitochondria accelerates chronic inflammation, leading to age-related conditions. Increasing calcium uptake in macrophages may help prevent harmful inflammation and its effects on the brain.
Scientists identified a process by which enzymes help prevent heart damage in chemotherapy patients. Enzymes normally found in mitochondria move to the nucleus, keeping cells alive. This discovery suggests new methods for testing individual patient responses and potentially preventing heart damage from chemotherapy.
Researchers at Tokyo Metropolitan University have discovered that 5-aminolevulinic acid can selectively boost Complex II and IV to counteract Complex I deficiency, a common cause of mitochondrial disorders. This finding offers new hope for the development of treatments for debilitating conditions such as MELAS syndrome.
Researchers at University of California San Diego find that impaired mitochondria, not inflammation, drive Gulf War illness symptoms, potentially leading to new treatment strategies. The study's findings have implications for other health conditions marked by increased inflammation.
Researchers found that ahiflower oil supplementation can recover mitochondrial respiration rates in honey bees exposed to imidacloprid, a common neonicotinoid pesticide. This study suggests the potential for food supplements to decrease honey bee mortalities caused by pesticides.