Articles tagged with Autophagy
HIV-associated neurocognitive disorders affect 10-50% of aging patients, causing cognitive impairment and daily challenges. Researchers found that the tat protein disrupts autophagy, a critical disposal process, in neurons.
Researchers found that autophagy, a cellular recycling process, helps eliminate a molecule called A20 that blocks the immune response. By removing A20, autophagy allows for a quick release of emergency signals, boosting anti-fungal immunity.
Researchers found that inactive EGFR is involved in autophagy, a process where cells consume nonessential contents to survive. Cancer cells use this process to thrive under stressful conditions. Combining drugs that block autophagy with those that inactivate EGFR could be an effective way to treat cancers
Researchers found that FKBP51 regulates acute and chronic effects of antidepressants via autophagic pathways in mice and humans. Autophagy markers correlate with antidepressant treatment response in patients with depression.
Researchers found that autophagy plays a central role in mediating the non-specific immune effects of BCG, leading to trained immunity. Monocytes from individuals with specific variants of the ATG2B gene respond with trained immunity, supporting the hypothesis that autophagy is clinically relevant.
Researchers found that autophagy, a cellular recycling mechanism, helps activate muscle stem cells by inducing metabolic shifts and coping with increased biosynthesis demands. Inhibited autophagy delayed stem cell activation, highlighting SIRT1's regulatory role in this process.
Scientists at Brigham Young University have discovered two proteins that trigger autophagy in cancer cells, offering a potential therapeutic avenue for targeted treatment. The study's unique approach led to the identification of a protein pair responsible for switching on autophagy under stress conditions.
Researchers at UC San Diego identified microRNA let-7 as a key player in managing cell survival and growth. The molecule controls autophagy through the amino acid sensing pathway, which has emerged as the most potent activator of mTORC1 complex activity.
Researchers identified a gene called AMPK that can slow the aging process throughout the entire body when activated remotely in key organ systems. Activating AMPK in fruit flies increased their lifespans by about 30 percent and kept them healthier longer.
Researchers at Virginia Commonwealth University Massey Cancer Center have developed a novel cancer therapy that leverages the autophagy defense mechanism to induce cell death in multiple myeloma cells. By targeting the p62 protein, the therapy disrupts autophagy and triggers apoptosis, resulting in increased effectiveness compared to t...
A study found that children with autism have a surplus of synapses in the brain due to a slowdown in synaptic pruning during development. The researchers discovered that administering a drug called rapamycin can improve autistic-like behaviors in mice, even when given after the behaviors have appeared.
Researchers found that autophagy is activated in the hippocampus of vascular dementia model rats, leading to neuronal injury. Inhibiting autophagy has shown neuroprotective effects, suggesting it as a novel pathway and target for drug treatment of vascular dementia.
Research suggests that autophagy may be both beneficial and detrimental to neuronal survival after stroke. The study proposes that autophagy has dual effects on neuronal survival, highlighting the need for further investigation into its therapeutic potential.
Quercetin reverses high glucose-induced inhibition of neural cell proliferation and reduces apoptosis through autophagy induction. Autophagic and proliferative activities are rescued in Schwann cells under high glucose conditions after quercetin intervention.
A team of researchers from UCLA discovered that autophagy, a process that clears damaged proteins, is impaired in people with Type 2 diabetes, leading to the destruction of insulin-producing beta cells. This impairment contributes to the accumulation of toxic IAPP protein.
Researchers found that an enzyme called acid sphingomyelinase (ASM) disrupts autophagy in patients with Alzheimer's disease, leading to toxic protein accumulation. Reducing ASM activity restored autophagy and improved memory in mice with AD-like disease.
Researchers have found that boosting autophagy, a cell-cleaning process, can help clear abnormal protein buildup in brain cells. Three drugs that enhance autophagy showed promise in keeping brain cells alive longer, potentially offering new treatment options for conditions like ALS and dementia.
Researchers have successfully blocked autophagy in a range of aggressive cancers, including glioblastoma, melanoma, and myeloma, using hydroxychloroquine. The study shows that combining autophagy inhibitors with other cancer therapies can be safe and effective for patients with very sick cancers.
Researchers found that treating cystic fibrosis patients with interferon gamma (IFN-γ) enhanced autophagy and cleared the lethal bacterial infection Burkholderia cenocepacia. This breakthrough offers new hope for patients with CF who are resistant to traditional antibiotics.
A study by Whitehead Institute researchers has identified a potential treatment for Niemann-Pick disease, a rare genetic disorder. The researchers found that combining low doses of cyclodextrin with the drug carbamazepine can lower cholesterol levels and restore autophagy defects in cells affected by the disease.
Researchers at the Weizmann Institute have discovered a new type of cellular vesicle that actively seeks out and destroys paternal mitochondria upon fertilization. This finding may help explain why only a quarter of IVF pregnancies carry to term, and could lead to a better understanding of mitochondrial turnover and male fertility.
Researchers discovered that nimotuzumab promotes autophagic cell death, enhancing the antitumor effects of chemotherapy and radiation in ESCC cells with high EGFR expression. This finding suggests a potential strategy for improving therapeutic efficacy in esophageal squamous cell carcinoma.
Researchers have identified a gene, PLAC-8, critical to pancreatic cancer progression and growth through autophagy. Inactivating the gene in mice significantly slows cancer's progression, offering a potential new route to treatment.
Researchers investigated the role of atrogin-1 in cardiac homeostasis and found that its deficiency promotes cardiomyopathy and premature death via impaired autophagy. Additionally, endothelial HIF-2 was shown to protect kidney from hypoxia-induced damage. These findings highlight the importance of protein turnover regulation and HIF-2...
Scientists have identified DOR protein as a plausible target against muscle deterioration in certain diseases. The researchers found that inhibition of DOR would only partially reduce autophagy, maintaining beneficial levels for cells.
A University of Colorado study shows that cancer cells can outlive chemotherapies by using autophagy, a process where cells recycle damaged parts. This finding has implications for developing drugs that inhibit autophagy to sensitize cancer cells to chemotherapy.
Researchers at the University of Texas MD Anderson Cancer Center found that blocking prolactin signaling can induce autophagy in cancer cells, leading to their death. In preclinical research, treatment with a prolactin-mimicking peptide reduced tumor weight by 50% and led to increased expression of autophagy genes.
Researchers found that the initial stage of autophagy is not directly related to the composition of the Beclin-1 complex. Instead, other mechanisms are likely involved in inducing autophagy. This study highlights the complexity of autophagy regulation and challenges current understanding of its role in neurodegenerative diseases.
Research reveals that lipid rafts are essential for the renewal of brain neurons in Alzheimer's disease by modulating the aberrant autophagic-lysosomal pathway. The study highlights a possible mechanism underlying the clearance of Alzheimer's disease products, implicating the autophagic-lysosomal pathway.
Neurons store glycogen as a rapid energy source, but excess leads to death. Conversely, small amounts are beneficial for cell survival during oxygen depletion.
Researchers found that a new preclinical study pinpointed a molecular mechanism in autophagy, spurring a clinical trial for patients with resistant melanoma. Blocking autophagy with the antimalarial drug hydroxychloroquine (HCQ) may enhance cancer cell death and improve outcomes for these patients.
A new study from Karolinska Institutet found that acidic tumor pH counteracts chloroquine's ability to inhibit autophagy in cancer cells. The results may explain the lack of efficacy of chloroquine in clinical studies, particularly in tumors with low oxygen and acidic pH.
Scientists at WashU Medicine have developed a new approach to treating muscular dystrophy, using nanoparticles loaded with rapamycin to improve recycling of cellular waste. The treatment showed significant improvements in skeletal muscle strength and cardiac function in mice with Duchenne muscular dystrophy.
A study found a link between a mutation in the RAB24 gene and canine hereditary ataxia, a neurodegenerative disease affecting dogs. The findings may help understand neurodegenerative diseases and identify new treatments for both canine and human sufferers.
Dr. Beth Levine received the 2014 Stanley J. Korsmeyer Award for her groundbreaking work on autophagy, a housecleaning process in which cells destroy damaged proteins and organelles. Her research has revealed crucial roles of autophagy in health and disease, including its potential to prevent cancer and neurodegenerative diseases.
A new study suggests that autophagy plays a key role in determining the fate of cancer cells when treated with anti-cancer drugs. Cells with high levels of autophagy were more susceptible to death from certain drugs, while those with low levels of autophagy were more resistant.
Researchers discovered reduced autophagy in schizophrenic patients' brains, which may lead to cell death. Boosting beclin 1 levels could restore balance and prevent harmful brain-cell death. ADNP levels were also found to be increased in the blood of schizophrenia patients.
A study published in the Journal of the American Society of Nephrology found that obesity increases the risk of developing chronic kidney disease by suppressing an important cellular process called autophagy. Restoring this process may help protect kidney health in obese individuals.
Researchers at RIKEN Brain Science Institute found that autophagy mediates the formation of amyloid beta plaques, a hallmark of Alzheimer's disease. The study suggests that autophagy might be a potential drug target for treating the disease.
Researchers from the University of Cambridge discovered that specialized intestinal cells called Paneth cells play a major role in inflammation underlying Crohn's disease. The study identifies autophagy as a key mechanism in removing ER-stressed membranes, which are rendered inflammatory by misfolded proteins.
UT Southwestern researchers discover that a protein overactivity sabotages cellular recycling, leading to heightened cancer growth and chemotherapy resistance. Autophagy inhibition may worsen chemotherapy outcomes for patients with specific cancer mutations, according to the study published in Cell.
A review article by Kesidou et al. explores the molecular mechanisms of autophagy and its role in chronic and acute neurodegenerative disorders. The study highlights the complex interplay between autophagy's protective and damaging effects, emphasizing the need for further research to fully understand its implications.
The study highlights the importance of autophagic and lysosomal activity in ischemic neurons, providing nutrition and energy for their survival. Upregulating cell autophagy or inhibiting autophagy may help eliminate abnormal components in cells after ischemic brain injury.
A recent study published in PLoS One reveals that impaired autophagy is linked to age-related macular degeneration, a leading cause of visual impairment. The researchers found that the lysosomal clean-up mechanism, or autophagy, plays a crucial role in clearing harmful protein accumulations behind the retina, which lead to vision loss.
Researchers at Sanford-Burnham Medical Research Institute have identified a critical transcription factor that regulates autophagy, a cleansing mechanism for cells. The discovery could lead to new therapies for age-related disorders by inducing autophagy in animal models and dietary-restricted mice.
Researchers at UT Southwestern Medical Center identified a novel mechanism by which Vibrio parahaemolyticus bacteria cause illness. The study reveals how the bacteria's effector protein, VopQ, disrupts autophagy by forming gated ion channels.
Autophagy, a process where cells consume parts of themselves to clean up damaged organelles and proteins, is controlled by a molecular switch in the cell nucleus. The study found that histone H4 acetylation regulates autophagy-related genes, offering new avenues for disease treatment.
Dr. Ken Cadwell has been recognized with the 2013 ICAAC Young Investigator Award for his exceptional research in infectious diseases and pathogenesis, with findings already having a profound impact on the fields of immunity.
Autophagy, a type of internal 'spring cleaning', helps maintain neural stem cells' readiness to become new brain and nerve cells. Without this process, these crucial stem cells suffer damage from waste products and their ability to differentiate diminishes.
Research shows that inhibiting autophagy in breast cancers dependent on it may be enough alone to kill the disease. Chloroquine, an anti-malaria drug, has been found to inhibit autophagy and is being tested as a potential treatment for certain breast cancer subtypes.
Researchers at Penn Medicine discovered that cells with low helicase-like transcription factor (HLTF) expression are more likely to respond to autophagy inhibition. This finding could lead to the development of a predictive biomarker for patients who may benefit from this treatment approach.
Researchers have discovered that Parkinson's disease protein, α-synuclein, forms insoluble aggregates that resist degradation in cells. The accumulation of these clumps impairs the macroautophagy system, a major garbage disposal system within the cell.
Laura Segatori, a Rice University engineer, has received a NSF CAREER Award to develop a toolkit for probing the workings of cellular processes that lead to diseases like Parkinson's. Her goal is to identify key proteins and learn how to regulate them using nanoparticles.
Researchers have found that a signaling molecule called SDF-1 helps stem cells survive in the low-oxygen environment of bone marrow by activating autophagy, a survival pathway. However, with age or disease, SDF-1's role shifts, reducing stem cell survival and increasing the likelihood of fat cell formation.
Researchers at Albert Einstein College of Medicine have discovered how the most common genetic mutations in familial Parkinson's disease damage brain cells. The study found that abnormal LRRK2 protein disrupts a 'garbage-disposal' process, leading to toxic levels of alpha-synuclein and neuronal death.
Researchers found that omega-6 fatty acids stimulate autophagy in both C. elegans roundworms and human cells, leading to increased lifespan and improved immune response. This discovery suggests that balanced intake of omega nutrients may benefit human health.
Researchers synthesized a peptide called Tat-beclin 1, which induces autophagy, a recycling process crucial for cell health. Mice treated with the peptide were resistant to several infectious diseases, including West Nile virus and HIV infection.
Researchers identify normalizing p62 levels in immune system cells as a strategy to clear an infection that is deadly to patients with cystic fibrosis. This approach enables the natural cellular process of autophagy, which helps digest pathogens and clear them away, thereby controlling inflammation and saving patients from death.
Autophagy is triggered when cells are starved for nutrients, infected, or damaged. The study reveals that AMPK regulates Vps34 kinase complexes in different ways, inhibiting non-autophagy enzymes and activating autophagic ones.
Whitehead Institute researchers identify Rag GTPases as key mechanistic regulators of autophagy, a process to break down internal energy sources. Rag GTPase's continuous activity leads to permanent activation of mTORC1, resulting in nutritional crisis and death in newborn mammals.