Researchers at Sanford Burnham Prebys discovered that blocking an energy transfer enzyme shifts mammalian hearts into a regenerative state, promoting regeneration and improving recovery after a heart attack. By modulating heart cell metabolism, scientists can potentially awaken the heart's dormant regenerative abilities.
Researchers uncover ancient energy-sensing signaling cascade in marine oysters that sheds light on human lung adenocarcinoma. The KAT2/HDACIIa–PGK–ALDO axis promotes glycolytic flux to ensure cell survival under energy stress.
A team of researchers at Ohio State University has identified a noncoding RNA that binds to ATP, which could lead to the development of new therapeutic nanomaterials. The discovery builds on previous work and follows up with an investigation into the mechanism of how this RNA binds to ATP.
Research reveals birds can harness lactate to rapidly resurrect blood function, outperforming mammals. Lactate enables bird RBCs to convert methaemoglobin back to haemoglobin three times faster than mammalian RBCs.
Scientists have identified a previously unknown genetic disease, MINA syndrome, which damages motor neurons and affects movement and muscle control. The disease is caused by a rare genetic mutation in the NAMPT protein, leading to symptoms such as muscle weakness, loss of coordination, and foot deformities.
Estrogen-related receptors play a crucial role in regulating muscle cell metabolism and energy production. Researchers discovered that these receptors can increase mitochondrial numbers and enhance energetic output when muscles need more energy, making them a promising therapeutic target for metabolic disorders.
Researchers discovered a promising new approach to treating hemorrhagic shock, which tripled survival rates and maintained healthy organ function. Activating Protein Kinase C epsilon (PKC-ε) significantly improved early survival rates and physiological stability following severe hemorrhage.
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.
Researchers have discovered how a mitochondrial pyruvate carrier transports a molecule vital for energy production into the cell's powerhouses. Blocking this process could lead to new treatments for various conditions, including diabetes, Parkinson's disease, and cancer.
Researchers at the University of Gothenburg have discovered a molecule that helps more mitochondria function properly, improving energy production in cells from patients with POLG mutations. This breakthrough paves the way for a new treatment strategy and may have broader therapeutic use for other mitochondrial diseases.
A new study from the University of Colorado Anschutz Medical Campus identified significant mitochondrial dysfunction in lymphoblast cell lines from children with Dravet syndrome, a severe form of epilepsy. The findings suggest that mitochondrial defects play a role in the metabolic dysfunction observed in Dravet syndrome.
Researchers at the University of Basel discovered that mitochondrial proteins assemble into large supercomplexes, crucial for providing cells with energy. These findings may lead to insights into human diseases and biotechnology applications.
Researchers at Sanford Burnham Prebys have discovered a way to target the energy supply chain of cancer cells. By understanding how enzymes like ubiquitous mitochondrial creatine kinase (uMtCK) function, scientists can design new treatments that slow or stop tumor growth.
Researchers at Amsterdam UMC and Moffitt Cancer Center found that contact with CLL cells leads to an energy crisis in T cells, making them unable to proliferate. The study suggests that restoring T cell energy could significantly enhance the effectiveness of current treatments for cancer.
A team of researchers from Japan directly visualized protein translocation across membranes for the first time, providing insights into the SecYEG-SecA complex dynamics and its role in facilitating protein movement. The study estimated a protein translocation rate of 2.2 amino acid residues per second.
A new mechanism by which brown fat is converted into heat has been identified, revealing a potential target for treating obesity and related metabolic diseases. The MCJ protein plays a crucial role in this process, protecting against health problems associated with obesity such as diabetes and increased blood lipids.
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.
A new study in Addiction Biology suggests that cannabis use can cause chromosomal damage, leading to increased cancer risk and birth defects. This genotoxicity may be transmitted to offspring via damaged sperm or eggs.
A new study from Karolinska Institutet found that people with type 2 diabetes have lower levels of the protein creatine kinase, leading to impaired mitochondrial function and energy production. This impairment may contribute to poorer energy metabolism in individuals with type 2 diabetes.
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.
Researchers at Texas A&M University have developed a method to recharge cellular mitochondria using nanotechnology, potentially extending healthy lifespans and improving outcomes for patients with age-related diseases. The molybdenum disulfide nanoparticles stimulate mitochondrial regeneration, helping cells generate more energy.
Researchers at the CNIC found that respiratory complex I possesses sodium transport activity essential for efficient cellular energy production. This discovery provides a molecular explanation for Leber's hereditary optic neuropathy and may have implications for other neurodegenerative diseases.
Researchers have discovered a new type of beige fat cells that consume energy and produce heat through a futile-cycle mechanism, known as the 'Sisyphus mechanism'. These cells are found in adults and help break down excess fat, leading to improved metabolic health and reduced risk of obesity.
A study published in Cardiovascular Research Journal found that a gene deficiency in patients with atrial fibrillation leads to reduced energy production in heart cells. PITX2-deficient cardiac cells have smaller and less efficient mitochondria, pushing the heart into an oxygen-deficient stress state.
A new study reveals that Meteorin-like protein saps energy from T cells, severely limiting their ability to fight cancer. By understanding this signaling pathway, researchers may be able to develop targeted treatments to restore metabolic health and enhance the immune system's power against tumors.
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.
Four studies conclude that longer genes are most susceptible to aging due to increased potential sites for DNA damage. Long genes have more sites for damage, making them prone to degradation with age, contributing to conditions like Alzheimer's disease.
A recent discovery reveals that the natural molecule trigonelline can increase NAD+ levels and improve muscle function during ageing. Lower levels of trigonelline were found in older people with sarcopenia, a condition where muscles weaken and mass is lost.
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.
Researchers found that a compound called BAM15 makes mitochondria less efficient at producing energy, extending life span and improving body composition in fruit flies. The study also showed reduced age-related decline in motor activity. Further studies are needed to confirm these findings in humans.
High levels of copper linked to poorer patient outcomes in clear cell renal cell carcinoma (ccRCC) patients, according to NIH-funded University of Cincinnati Cancer Center research. The study aims to identify copper's mechanisms and test potential new treatments for ccRCC.
Scientists engineered yeast that can harness energy from light, growing 2% faster in the light than in the dark. This discovery provides key evolutionary insights into how rhodopsins spread across lineages and has potential applications for biofuel production and studying cellular aging.
A recent study published in Nature Communications found that Long-COVID patients experience fatigue due to reduced energy production by mitochondria in muscle cells. The research suggests a biological cause for the persistent exhaustion, opening up potential treatment avenues.
A new Duke University-led study finds that Gulf War Illness significantly reduces the ability of white blood cells to make energy, creating measurable biochemical differences in veterans with the disease. The study reveals impaired mitochondrial function, leading to lower levels of extracellular acidification and oxygen consumption.
A significant breakthrough sheds light on Parkinson's disease mechanisms, revealing that mitochondrial DNA damage triggers the spread of debilitating symptoms. The researchers' findings offer promising potential for innovative treatments and diagnostics.
The study found that black soldier fly larvae oil exhibits anti-inflammatory properties, suppressing proinflammatory cytokines and improving colon health. BSFL oil's unique compound profile may offer a new approach to managing inflammatory diseases.
Mutations in parkin gene break down contacts between lysosomes and mitochondria, disrupting essential metabolite supply to mitochondria. Restoring these contacts may represent a new therapeutic opportunity for Parkinson’s disease.
A molecular switch called Arf1 controls the storage or conversion of lipids into energy in cells. When energy is needed, Arf1 allows lipids to enter mitochondria, where they are converted into ATP.
The nucleus is metabolically active and uses antioxidant enzymes to repair DNA damage. Cells relocate mitochondrial machinery to the nucleus in response to DNA damage, highlighting a paradigm shift in cellular biology.
A study by CNIC researchers reveals that gamma-linolenic acid in breast milk binds to the retinoid X receptor protein, activating gene expression and influencing biological functions. This activation initiates genetic programs that equip mitochondria with the necessary enzymes and proteins to start consuming lipids as energy.
Researchers discovered that FDA-approved HDAC-inhibitors can impact energy metabolism in solid tumor cells, including glioblastoma. The combination of HDAC-inhibitors and imipridones may synergize to enhance killing of GBM cells by reversing cellular respiration.
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.
Scientists at Duke University found electric fields within biological condensates, which could change the way researchers think about biological chemistry. The discovery suggests that these structures may have played a crucial role in the first life on Earth, providing energy for essential reactions.
Researchers discover that brain cells die from lack of energy when autophagy, a natural cleaning process, malfunctions. Compounds boosting NAD levels can improve neuron survival and combat age-related neurodegeneration.
Researchers uncover the critical link between cellular energy levels and mitochondrial damage through protein FNIP1. The study reveals that FNIP1 enables communication between AMPK and TFEB, instructing genes to remove damaged mitochondria and create new ones.
Researchers at Gladstone Institutes have made a groundbreaking discovery about how neurons consume and metabolize glucose, a process crucial for maintaining normal energy levels. The study found that neurons rely on glycolysis to break down glucose, and its disruption can lead to severe learning and memory problems in mice.
A new study by Van Andel Institute scientists identifies KDM5C as a key driver of low bone density, preserving bone mass in mice. The discovery may lead to more effective treatments for women with osteoporosis, reducing the risk of fractures and improving quality of life.
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.
The study resolves a long-standing question about the structure of respiratory supercomplexes in unicellular eukaryotic organisms. Complex II is found to be part of the supercomplex in these organisms, optimizing ATP formation and revealing a surprising variety in supercomplex construction.
Researchers developed a small-molecule drug that limits magnesium transport into cellular power plants, resulting in skinny, healthy mice. The findings hold significant implications for preventing cardiometabolic diseases like heart attack and stroke, as well as reducing liver cancer risk.
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 at NTU Singapore have found a way to spur brain immune cells to clear toxic waste linked to Alzheimer’s disease by targeting their metabolism. The study reveals a ‘metabolic switch’ in the brain’s immune cells that can be manipulated to improve their function.
Researchers found that suppressing AMPKα1 but not AMPKα2 isoforms improved aging-related impairments in mice. The study revealed novel insights into the roles of AMPK signaling pathway in cognitive aging.
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 genetically engineered mitochondria to convert light energy into chemical energy, increasing ATP production and lifespan by 30-40%. The study provides new insights into mitochondrial function and offers a platform for studying age-related diseases.
Researchers discovered that starvation causes changes in endoplasmic reticulum (ER) structure in human cells, leading to impaired mitochondrial function and severe energy deficiency. This mechanism is crucial for understanding the progression of X-linked centronuclear myopathy.
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 novel synthetic energy system supports yeast cell growth and produces highly reduced chemicals, achieving high yields of biofuels. The system's reductive metabolism enables efficient energy production, overcoming stoichiometric constraints and outperforming natural metabolic processes.