Articles tagged with Mitochondrial Function
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Researchers have identified ATAD3A as a molecular determinant that favors the development of head and neck cancer. The protein is involved in various cellular processes, including energy metabolism and apoptosis. Targeting ATAD3A could offer a novel approach to developing effective anti-cancer therapeutics.
Researchers at Salk Institute discover that dysfunctional mitochondria at synapses fail to meet energetic demand, supplying either too much or too little power and potentially causing working memory impairment with age. Adherence to the ultrastructural size principle is essential for avoiding cognitive decline in aging brains.
Researchers found that a mutation in the SKD3 enzyme can cause 3-methylglutaconic aciduria (MGCA7), a genetic disorder associated with variable neurologic deficits and low neutrophil count. The mutation leads to protein aggregation and inactivates the enzyme, disrupting mitochondrial function.
A study found that regular exercise increases mitochondrial fusion, benefiting muscle cells and maintaining physical fitness even in old age. Daily sessions of exercise throughout life delay the accumulation of dysfunctional mitochondria and decline in physical fitness.
A massive supercomplex in mitochondria comprising all four respiratory complexes induces a membrane curvature necessary for proper mitochondrial function. The supercomplex assembly actively contributes to the shaping of the macroscopic architecture of mitochondria.
Researchers have identified a molecule called NLRP10 as an intracellular 'smoke detector' that warns of mitochondrial damage. This detection triggers a process that eliminates damaged cells, preventing chronic inflammation and tissue damage. The discovery could lead to new therapies for skin and intestinal diseases.
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 has provided systematic insight into the organization of proteins in mitochondria, a crucial cell compartment responsible for energy production. The researchers created a high-resolution image of the organization of mitochondrial proteins using complexome profiling, revealing protein complexes that enable cellular processes.
Researchers found abnormal 12-hour gene activity cycles in postmortem brains of patients with schizophrenia. The study identified altered timings of neural connections and mitochondrial function, suggesting potential underlying causes for behavioral abnormalities.
Researchers found that SIRT6 maintains mitochondrial function through transcription regulation of mitochondrial genes. Without SIRT6, mitochondrial gene expression is down-regulated, leading to increased ROS production and impaired ATP generation, similar to changes observed in aging and neurodegenerative diseases.
Research reveals that commonly used antiretroviral drugs TAF and TDF directly impact mitochondria's energy production in immune cells. The study suggests a larger energy reduction when combined with other antiretrovirals, sparking concerns about potential long-term effects on human cells.
Researchers at La Jolla Institute for Immunology have discovered that OGT regulates mTOR, a key protein for mitochondrial powerhouses, keeping cells healthy. The study may lead to important medical advances in understanding cancers, diabetes, and cardiovascular disease.
Researchers at the University of Freiburg and Kyoto Sangyo University have elucidated the guidance mechanism for mitochondrial pore formation through structural and functional experiments. The study reveals that Sam50 and Sam37 proteins play critical roles in forming barrel pores, essential for cellular function.
A new study by RCSI University of Medicine and Health Sciences found that the circadian body clock influences immune responses to vaccines. The research discovered that the shape of mitochondria in dendritic cells changes throughout the day, impacting their ability to break down vaccines.
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.
A new study found that gestational exposure to the flame retardant FM 550 resulted in altered brain development in newborn rats, with effects more pronounced in male offspring. The study also showed evidence of mitochondrial disruption and dysregulated choline and triglyceride levels in brain tissue.
Researchers at the University of Alabama at Birmingham have identified TBX20 as a vital regulator of direct human cardiac reprogramming. Adding TBX20 to existing cocktails improves contractility and mitochondrial function in reprogrammed heart muscle cells, suggesting a therapeutic potential for TBX20.
A new study has discovered that MTCH2, a protein essential in various cellular processes, acts as a 'door' for proteins to access the mitochondrial membrane. The finding opens up potential avenues for cancer treatments by harnessing apoptosis, a programmed cell death mechanism.
Researchers at Massachusetts General Hospital and Children's Hospital Philadelphia have identified a rare genetic disorder affecting mitochondrial energy production. The study found that identical twins exhibited hypermetabolism due to hyperactive mitochondria, resulting in low body weight despite consuming more calories than needed.
A new study led by Erika Pearce at Johns Hopkins Medicine found that the shape and function of mitochondria in Th17 cells play a crucial role in controlling their autoimmune activity. The researchers identified several molecules, including LKB1, that can influence this process, paving the way for potential therapeutic modifications.
Scientists have successfully delivered a common blood pressure medication directly to the inner membrane of mitochondria, targeting energy-producing parts of cells. The new method uses the body's natural transport system to deliver drugs more precisely, potentially improving therapy efficacy and reducing negative side effects.
Scientists have discovered a potential path against inherited neurodegenerative diseases by increasing the activity of TRAP1, which promotes mitochondrial protein-folding and corrects lysosomal dysfunction. This approach may have implications for treating multiple disorders affecting the central nervous system.
Researchers at UB have discovered a connection between mitochondrial defects and the shortening of telomeres, a key biomarker of premature aging. The study used a novel technique to restore normal function to abnormal mitochondrial interactions, providing potential avenues for diagnosis and treatment.
University of Cincinnati researchers have discovered a technique using light-activated proteins to normalize dysfunctional mitochondria in cells. This method has the potential to treat certain diseases, including cancer and neurodegenerative disorders.
Researchers found that COVID-19 patients produce fewer ketone bodies than influenza patients, leading to reduced immune function. A ketogenic diet or administering ketone bodies revived immune cells in diseased mice, improving virus elimination and lung damage.
A genetic defect in flies leads to motor disorders, similar to those found in humans with Parkinson's disease. The study suggests that Creld, a protein involved in energy production, may play an important role in the development of Parkinson's.
Scientists have identified a new pathway for peroxisome division, independent of Mitochondrial Fission Factor (MFF). The study, led by Professor Michael Schrader, reveals that PEX11β and FIS1 cooperate to divide peroxisomes, restoring normal morphology. This discovery offers potential therapeutic options for diseases caused by defects ...
Researchers discovered a novel mechanism by which non-coding 7S RNA regulates mitochondrial gene expression in human cells. The study found that 7S RNA inhibits transcription via mitochondrial RNA polymerase dimerization, shedding light on the molecular basis of this process.
Research reveals pridopidine enhances autophagy in ALS model, reducing toxic protein aggregation and promoting neuronal health. The study supports pridopidine's potential as a treatment for neurodegenerative diseases like Huntington's disease and Alzheimer's.
Researchers have identified the genetic causes of three mitochondrial diseases and proposed 20 additional possibilities for further investigation using a new approach. The study provides a platform to better understand how mitochondria's hundreds of proteins work together, which could lead to improved diagnoses and treatments.
Research finds that excessive mitochondrial damage caused by alcohol exposure can lead to chronic liver disease. Mitochondrial depolarization triggers mitophagy, a process removing damaged mitochondria; however, constant removal causes additional liver tissue damage.
A new clinical study published in Cell Reports Medicine found that daily intake of postbiotic Urolithin A improved muscle strength by 12% in middle-aged adults. The supplement supported the cells' ability to renew their powerplants, the mitochondria, during the aging process.
A new Cambridge study has discovered that the sex of a fetus can affect placenta function, diet-induced maternal obesity, and stress. Designing sex-specific therapies and personalized lifestyle interventions could have lifelong health benefits for children.
Researchers discovered that lipid droplets play a crucial role in mitochondrial recycling, and impairing DGAT1 activity leads to reduced recycling and increased cell stress. The study provides new insights into iron homeostasis and its impact on cellular metabolism.
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 research team found that limiting energy in neurons increases hyperexcitability and severity of seizures in mice. The ketogenic diet restored mitochondrial function and reduced seizure intensity.
Researchers from IRB Barcelona have discovered that damaged mitochondria accumulation triggers inflammatory processes leading to muscle atrophy. Correcting mitochondrial function through increased BNIP3 levels can mitigate inflammation and muscle loss, offering potential tools for promoting healthy ageing.
A team of scientists led by Karine Le Roch has identified two proteins, RAP01 and RAP21, crucial to the malaria parasite's survival. Knocking down these proteins can interrupt protein translation in the mitochondria, leading to the parasite's death.
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.
A new University of Copenhagen study reveals that well-functioning fat tissue is crucial for overall health and may help prevent diseases such as type 2 diabetes, cancer, and obesity. High levels of lifelong exercise have been shown to improve mitochondrial function in fat cells, reducing oxidative stress and damage.
A review published in Journal of Internal Medicine suggests that micronutrient supplementation could represent an effective treatment for heart failure. Micronutrients like iron, selenium, zinc, and coenzyme Q10 can impact cardiac cells' energy production, contributing to the disease.
A dietary supplement combining 5-aminolevulinic acid and sodium ferrous citrate helps slow down aging-related muscular decline in fruit flies. The study reveals improved muscle architecture and mitochondrial function, offering a potential therapeutic option to address age-related muscle health.
Researchers found that CBN preserves mitochondrial function and prevents oxidative damage to nerve cells, suggesting potential for treating age-related neurodegenerative diseases like Alzheimer's. The compound works independently of cannabinoid receptors, making it a promising therapeutic option.
Scientists have mapped the tau interactome, showing that mutant tau impacts mitochondria function in human neurons. The study also reveals a mechanism for tau release from neurons and its binding to mitochondrial proteins, which may inform future studies on preventing diseased tau spread.
A study found that a daily supplement of urolithin A improved muscle function and reduced inflammation in older adults. The supplement, produced by gut bacteria, was shown to stimulate mitophagy, a process that recycles damaged mitochondria.
Researchers at National Jewish Health have discovered that mitochondria do not function properly in patients with post-COVID syndrome, leading to debilitating symptoms. The study's findings may lead to treatments for patients struggling with fluctuating heart rates, extreme fatigue and memory issues.
Researchers discovered that pathogens can hijack mitochondrial defense mechanisms by mimicking host proteins, effectively disarming the mitochondria. This allows the pathogen to acquire essential nutrients and evade the host's immune response.
Exercise modifies the adaptation of the liver to increased energy intake, regulating enzymes for glucose and fructose degradation. Regular physical activity also improves glucose control and reduces fat storage in the liver, offering a comprehensive insight into molecular adaptations to high-energy diets.
Researchers at Kobe University discover that adding Vitamin B2 to stressed cells increases mitochondrial energy production and prevents cellular senescence. This finding has potential implications for preventing age-related disorders and extending healthy lifespans.
Researchers discovered that wound macrophages undergo different metabolic programs to coordinate tissue repair, including the use of reactive oxygen radicals for blood vessel growth. Macrophages also utilize a different type of mitochondrial exchange for anti-inflammatory and reparative functions in late-stage wound healing.
Researchers at Tel-Aviv University have shed light on the Sigma-1 receptor's topology and function in neurodegenerative diseases. The study reveals that the receptor is retained in the endoplasmic reticulum and its amino end faces the cytoplasm, providing a crucial mechanism for therapeutic approaches to alleviate suffering from ALS.
A study found that D-glyceric acid treatment improved metabolism, blood parameters, and reduced low-grade inflammation in healthy volunteers aged 50-60 years. The compound's activation of mitochondrial metabolism may help interrupt the spiral of persistent systemic inflammation and improve liver function.
Researchers discovered that altering macrophage metabolism helps prevent overloading and resolves inflammation by protecting mitochondria from strain. This process enables efficient removal of damaged cells, a key factor in resolving inflammation.
Researchers at Salk Institute discovered that long-lived mitochondrial proteins remain stable for an extended period, protecting them from damage. This stability allows these proteins to maintain mitochondrial function even when new ones are synthesized, providing protection against errors and energy-conservation benefits.
Researchers have discovered that increasing Telomerase Reverse Transcriptase in mitochondria improves mitochondrial function and reduces damaged area after a heart attack. This leads to better recovery of cardiac function and protection against cell death.
Dysfunction in mitochondrial respiration leads to imbalanced extracellular matrix (ECM) and tissue organization in cartilage. Research discovered the respiratory chain plays a key role in maintaining ECM balance.
Researchers successfully mimic nano spatial compartments to create artificial mitochondria, capable of supplying ATP or other useful molecules to cells in damaged or diseased tissues. The artificial organelles are generated from Exosome fusion and can function as energy reserves in the damaged tissues.
Researchers found that Parkin, a tumor suppressor, blocks tumor growth and invasion by inhibiting metabolic reprogramming and mitochondrial function. This study demonstrates that altering cancer cell metabolism is a potent driver of disease.
A study by Van Andel Institute scientists found that surplus sugar causes mitochondria to become less efficient, reducing their energy output. A low-sugar ketogenic diet reversed this effect, supporting healthy mitochondrial integrity and function.
Pridopidine's neuroprotective effects are supported by new research that elucidates its mechanisms through activation of the Sigma-1 Receptor (S1R). The study highlights pridopidine's therapeutic potential and provides data supporting the role of S1R in neurodegenerative diseases.