Articles tagged with Cell Death
Researchers discovered that vitamin K acts as an antioxidant, inhibiting ferroptotic cell death and identifying FSP1 as the warfarin-insensitive enzyme responsible. This finding has implications for treating Alzheimer's disease and acute organ injuries.
A recent study published in Movement Disorders found that a buildup of TDP-43 protein may be responsible for PD-related cell death. This discovery suggests a new cause of the disease and could lead to the development of new treatments.
A team from UNIGE has identified a molecular mechanism that causes degeneration of photoreceptors in retinitis pigmentosa, a genetic disease leading to blindness. The discovery could lead to therapeutic treatments targeting this mechanism.
Researchers at Johns Hopkins Medicine identified a chemical compound that stops the final events in the pathway linked to brain cell death in Parkinson’s disease. The compound, PAANIB-1, blocks the protein parthanatos without affecting its other critical activities, potentially halting neurodegenerative progression.
Researchers have discovered a membrane lipid called PI(18:1/18:1) that significantly involves in preventing programmed cell death. This finding opens up new therapeutic approaches for diseases such as diabetes, cancer and neurodegeneration.
Researchers have identified a new enzyme, tankyrase-1, that regulates cell death in inflammatory diseases like psoriasis. The discovery may lead to more effective treatments for chronic inflammatory conditions, some cancers, and viral infections.
A new mathematical theory explains how cells navigate the risk-speed tradeoff when dividing, balancing risk and speed to ensure survival. The theory applies broadly to all organisms, despite differences between yeast and mammalian cells.
A FSU study found that brown spots on bananas appear during a two-day window, expand rapidly, then stall, leaving distinct patterns. The researchers developed a model describing the speed of reaction and oxygen movement, which may help tackle food waste by understanding the browning process.
Researchers have identified a new type of programmed cell death, erebosis, that takes place in the intestines of fruit flies, contradicting the long-held theory of apoptosis. The process involves gradual cell death without nuclear membranes, mitochondria, and cytoskeletons, and is thought to play a role in gut metabolism.
Scientists at University of Illinois and Mie University develop monoclonal antibodies to prevent lung cell death in mouse models of idiopathic pulmonary fibrosis and acute respiratory disease syndrome. Non-invasive diagnostic tools also presented could aid in predicting disease progression and identifying patients at risk.
Researchers found that brains from patients with Alzheimer's disease had higher levels of the protein Fli-1 and fewer pericytes lining their smallest blood vessels, leading to leakage. Blocking Fli-1 improved memory in mice, suggesting a promising new approach to treating the disease.
Dr. Zhiqiang Lin has been awarded a $3.2 million NIH grant to investigate the roles of YAP and IRF2BP2 in the cardiac innate immune response, with the goal of reducing cardiac inflammation and promoting heart recovery after a heart attack.
A U-M study defines how a cytokine and fatty acid combination triggers ferroptosis, a type of cell death previously studied with synthetic molecules. This natural mechanism could make immunotherapy treatments more effective, particularly for cancers where the treatments currently work for only about 30% of patients.
Scientists have developed a new therapy called CINDELA, which employs CRISPR-Cas9 to kill cancer cells while leaving normal tissues intact. The treatment targets specific mutations found in cancer cells and induces cell death through DNA double-strand breaks.
A preclinical study identified a protein complex critical for regulating apoptosis and necroptosis. Inhibiting this complex may help prevent excessive cell death and tissue damage associated with heart attacks, autoimmune disorders, and COVID-19. Researchers believe that targeting the PPP1R3G/PP1γ pathway could lead to new treatments f...
Researchers have identified nitric oxide as a key driver of excessive cell death and inflammation in the body. By blocking caspase-8, a protein that produces nitric oxide, unregulated cell death can be prevented, offering new treatment options for inflammatory diseases.
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.
Researchers at the University of Illinois Chicago have developed a new method for analyzing pyroptosis, a process of cell death previously thought to be irreversible. By using optogenetic gasdermin, they found that certain conditions can trigger pores to close within tens of seconds, suggesting the process dynamically self-regulates.
Researchers have visualized the first structure of a human cell death complex linked to autoimmune and inflammatory diseases. The discovery could lead to new treatments for inflammatory bowel disease, renal injury, diabetes, and other conditions. The study reveals how RIPK3 proteins regulate necroptosis, a type of inflammatory cell death.
Researchers developed a new technology that tracks thousands of cells and determines the precise moment of death for any cell in the group. The approach was shown to work in rodent and human cells as well as within live zebrafish, and can be used to follow cells over weeks to months.
Scientists from Okayama University have identified the genes that cause pesticide sensitivity in sorghum, a superfood grain. The study reveals that these genes are involved in plant defense mechanisms and could help develop crops that can be grown safely with organophosphate treatment.
Researchers from Kazan Federal University have developed a gene-cell preparation that uses membrane vesicles to target and kill cancer cells. The technology has shown promise in treating various types of cancer, including breast, lung, and colon cancer.
Researchers describe disassembly of Drosophila fly trachea during metamorphosis, revealing two-stage process involving cell shrinkage and death. The study highlights intricate involvement of physical mechanisms and biological signalling in regulating cellular decisions.
A recent study published in Cell Metabolism found that reducing naturally occurring errors in protein synthesis improves both health and lifespan. By engineering a mutation in ribosomes, researchers observed fewer protein mistakes and improved heat resistance, leading to longer lifespans in yeast, worms, and fruit flies.
A recent study explores the plant immune system using chimeric maize leaves with an auto-active R protein. Researchers found that Rp1-D21 triggers a defense response without recognition events, leading to cell death in affected areas but not neighboring cells.
Researchers have uncovered a weakness in the key enzyme that solid tumour cancer cells rely on to adapt and survive when oxygen levels are low. Inhibiting this enzyme, called Carbonic Anhydrase IX (CAIX), can effectively stop cancer cell growth.
Researchers have discovered that inhibiting the GOT1 enzyme can promote ferroptosis, a type of programmed cell death, in pancreatic cancer cells by conserving nutrients and releasing iron stores. This study provides a new potential therapeutic target for treating pancreatic cancer.
Researchers at the University of Texas M.D. Anderson Cancer Center have discovered that targeting the mitochondrial enzyme DHODH can induce ferroptosis and suppress tumor growth in cancer cells. The study suggests a new therapeutic strategy for inducing ferroptosis, which could have broad implications for treating various types of cancer.
Researchers designed a simple screening assay based on competitive binding to identify peptide candidates with high binding affinity for ubiquitin. The dimers of cyclic peptides were found to be more potent than control peptides and induced cell death in live cancer cell lines.
Researchers have discovered a way to prevent cell death in the hearts of people with arrhythmogenic cardiomyopathy (ACM), a genetic disease that can lead to sudden cardiac death. By inhibiting two mitochondrial proteins, cell death can be prevented, offering new therapeutic options for those affected.
A study in mice suggests that iron processing in the body may contribute to heart failure, and blocking this process could be a way of protecting the heart. Researchers found that inhibiting the release of stored iron can reduce cell death and stabilize oxygen levels.
Researchers found that loperamide triggers autophagic cell death in glioblastoma cells by inducing ER stress, opening new avenues for treatment strategies. The mechanism may also be applicable to other diseases where ER degradation is disrupted.
Researchers used the MADM technique to investigate how cells respond to changes in genomic imprinting. They found that cells activate certain gene groups involved in cell death, growth, and synapse development, particularly in astrocytes.
Researchers develop gold nanoparticles that selectively inhibit extrasynaptic glutamate receptors, preserving neurotransmission while blocking excessive activation. This breakthrough offers promising perspectives for targeted therapy without major side effects.
Researchers have found that ZBP1 is activated by Z-form nucleic acids in the absence of viral infection, leading to cell death and inflammation. Endogenous retroelements may be a source of these nucleic acids, triggering this mechanism in humans.
Researchers have identified a link between the nervous system and immune system in Parkinson's disease, finding that genes like Parkin and PACRG protect nerve cells from cell death. These proteins regulate a signalling pathway that also plays a role in innate immunity, which prevents bacterial infections.
New research suggests that moving birth a day early can trigger an early start to widespread neuron death in the developing brain. Delaying birth has no apparent effect on when this cell death occurs, indicating a developmental process takes over in this scenario.
A new human autoinflammatory disease called CRIA syndrome has been discovered and identified by an Australian-US research team. The disease is caused by a mutation in the RIPK1 protein, leading to uncontrolled cell death and inflammation.
A new study suggests that high glucose levels increase enzymatic precursor lysyl oxidase propeptide (LOX-PP), promoting cell death and contributing to retinal vascular cell loss. LOX-PP may be a therapeutic target for developing novel treatments for diabetic retinopathy.
Researchers at Karolinska Institutet found that only viable neurons survive in the developing nervous system, while immature ones die. This discovery challenges the long-standing neurotrophic theory and could lead to new treatments for neurological diseases like Parkinson's.
A new developmental mechanism, interdigital cell death, shapes limbs through differential growth and ROS production. This mechanism is shared by all amniotes, including humans, and was triggered by high oxygen levels surrounding the embryo.
Researchers found that atmospheric oxygen exposure triggers removal of interdigital webbing during embryo development. This mechanism is thought to be shared by all tetrapods and contributes to limb shape variation. The study provides insight into the evolutionary process behind limb development in animals.
Researchers identified a new molecular mechanism causing rheumatoid arthritis, finding that death of macrophages triggers the disease. The protein A20 was found to prevent macrophage death and protect against arthritis.
Researchers investigated nanomaterials' potential to activate the body's antitumor immune response. The study found that biomaterials can induce immunogenic cell death, leading to a decrease in metastases and an increase in long-term survival rates.
Researchers found that vaginal births reduce cell death in brain regions, while C-sections lead to increased ultrasonic vocalizations and altered hormone expression at weaning. Cesarean-born mice also had greater body weight.
Researchers found greater nerve cell death in Cesarean-born mice, associated with reduced neurons and altered behavior, but no effect on overall brain size or development
Researchers found that lysophosphatidic acid levels increase after traumatic brain injury, particularly in areas associated with cell death and axonal injury. Elevated LPA may serve as a biomarker for TBI through blood testing, providing a prognostic indicator of injury and outcome.
Researchers create nanoaggregates of microtubules by controlling their aggregation in response to light. The aggregation can cause cell death, making it a potential target for diseases caused by protein misfolding.
Scientists at Stanford University School of Medicine have identified a molecular code that unleashes necroptosis, a violent form of cell death. The discovery opens the door to potential new treatments for diseases such as inflammatory bowel disease and multiple sclerosis.
Researchers discovered that grapes experience internal oxygen shortage during ripening, leading to cell death and potentially affecting wine quality. The study's findings suggest that manipulating oxygen supply can reduce cell death, and may lead to new ways of selecting grape varieties for warmer climates.
Researchers have developed a water-soluble warped nanographene molecule that induces cell death when exposed to blue laser light, showing promise for fluorescent cell imaging and possibly eradication of cancer cells. The molecule exhibits green fluorescence under ultraviolet or blue light and has low cytotoxicity.
Trans-fatty acids directly activate ASK1 kinase by enhancing extracellular ATP, promoting cell death in a more direct manner than previously thought. The study identifies several trans-fatty acid types that stimulate cell death, but not their corresponding cis-fatty acids, which have health benefits.
A Brown University study used a custom-built device to compress neurons in 3-D cell cultures and observed their reaction to traumatic brain injury. The findings suggest that there may be a window for therapeutic intervention aimed at minimizing further damage, with irreparable structural damage occurring after approximately six hours.
Researchers have visualized how immune cells create networks of DNA traps called NETs to capture and destroy microbes. The process, known as NETosis, involves the transformation of histones and release of digestive enzymes into the extracellular space.
A new method detects multiple diseases via methylation patterns of circulating DNA from dying cells, identifying cell death in specific tissues and offering a minimally-invasive window for monitoring and diagnosis. The approach has vast possibilities for diagnostic medicine and can be adapted to identify cfDNA derived from any cell type.
A recent clinical study found that ONC201 caused cell death in various tumor types, even when the p53 protein was mutated or deleted. The drug has shown promise in treating hematological malignancies, including leukemia and lymphoma patients, with clinical trials recently initiated.
A study found that aspirin's breakdown product salicylic acid blocks cell death associated with Alzheimer's, Parkinson's and Huntington's disease by inhibiting the GAPDH enzyme. Derivatives of salicylic acid may hold promise for treating multiple neurodegenerative diseases.
Researchers at York University have discovered that beta-blockers may prevent further cell death following a heart attack, potentially leading to better long-term patient outcomes. The study found that the protein complex MEF2 plays a key role in heart cell survival and gene expression.
Researchers have discovered the molecular culprits behind primary open-angle glaucoma, a leading cause of blindness, by identifying two key risk genes: SIX6 and P16. The study found that high eye pressure increases expression of P16, linking it to increased risk of vision loss.
Scientists have identified a gatekeeper enzyme that prevents cell death in Wolfram syndrome, a rare form of diabetes. Replacing or enhancing the enzyme strengthens cellular membranes and stops molecules from leaking into other parts of the cell.