Articles tagged with Cell Death
A newly developed compound called UH15-38 has been shown to safely and efficiently block necroptosis, a key receptor in lung cells causing excessive inflammation and lung damage. The study demonstrates that UH15-38 can prevent influenza deaths even when administered late in the course of an infection.
Researchers have discovered that a rare type of lipid, with two polyunsaturated fatty acyl tails, promotes ferroptosis, a form of cell death. This finding could lead to new treatments for neurodegenerative diseases and induce cancer cell death.
A novel drug principle has been successfully tested in a mouse model and brain organoids of ALS patients, preventing cell death and improving motor abilities. The discovery of the TwinF interface inhibitor FP802 offers a promising path for fighting ALS and could lead to the development of effective treatments.
A team of scientists has found that 7-dehydrocholesterol (7-DHC) integrates into cell membranes and prevents ferroptosis, increasing cellular fitness and potentially promoting aggressive cancer behavior. This discovery could lead to the development of new cancer treatments targeting cholesterol biosynthesis.
Researchers at Northwestern University have discovered that toxic short RNAs contribute to neuron death and DNA damage in Alzheimer's disease. Studies found that older individuals with superior memories have higher amounts of protective short RNA strands in their brains.
Researchers identified gartisertib as a potent ATR inhibitor that enhances cell death in patient-derived glioblastoma cell lines. The study also showed synergy between gartisertib and TMZ+RT treatment, with higher sensitivity to gartisertib observed in MGMT promoter unmethylated cells.
A pioneering study published in The American Journal of Pathology reveals the cytoprotective and proregenerative effects of neuropeptide α-MSH in promoting corneal healing after eye injury. The treatment has shown impressive therapeutic potential in reducing the need for corneal transplants.
A team of researchers discovered a multiprotein complex involving NLRP3, AIM2, NLRC4, and Pyrin that drives PANoptosis, a type of programmed inflammatory cell death. The findings have implications for understanding inflammasome biology and identifying potential therapeutic targets.
Researchers explore the properties of cytostatic persisters in cancer treatment, highlighting their therapeutic potential and challenges. The study suggests that targeting these persisters before resistance emerges can reduce cancer recurrence.
José Pedro Friedmann Angeli, a pioneer in ferroptosis research, has received the ERC Consolidator Grant to explore key metabolic pathways. His project aims to decipher and exploit ferroptosis regulatory mechanisms in cancer.
Researchers from Columbia University have validated GLS2's ability to promote ferroptosis in murine models. This study suggests that targeting GLS2 may be a potential therapeutic strategy against liver diseases, particularly hepatocellular carcinoma.
Researchers identified a 'guard mechanism' controlling protein GPB1 to attack microbes and cancer cells. The study found that disrupting this mechanism can kill pathogens like Toxoplasma and potentially treat cancer.
Researchers at Chalmers University of Technology have shown that graphene oxide nanoflakes can reduce the accumulation of misfolded amyloid peptides in yeast cells, which are similar to human neurons affected by Alzheimer's disease. This suggests that graphene oxide may hold great potential for treating neurodegenerative diseases.
Researchers at Northwestern University identified a new evolutionarily conserved RNAi-based form of cell death called Death Induced by Survival gene Elimination (DISE), which targets essential survival genes in cancer cells. This mechanism is ancient and effective against all cancers tested.
Researchers found that a genetic variation in the MLKL gene is carried by up to 3% of the global population, increasing the risk of inflammation and related diseases. This discovery may lead to personalized treatments for conditions like inflammatory bowel disease.
A new study in PNAS discovers a protein, Iditarod, that regulates autophagy in fruit flies, linking exercise to cellular maintenance and cold tolerance. Flies lacking the gene exhibit impaired exercise endurance and reduced ability to tolerate cold.
Researchers found that ferroptosis, a form of cell death caused by iron buildup, destroys microglia cells in the brain's immune response, contributing to cognitive decline. The study's findings may lead to the development of compounds targeting microglial degeneration, offering new hope for Alzheimer's and vascular dementia treatments.
Researchers discovered a unique mechanism in naked mole-rats that targets senescent cells, suppressing their accumulation and delaying aging. This 'natural senolytic' process involves serotonin metabolism and oxidative stress, potentially offering an evolutionary rationale for removing senescent cells as a therapeutic strategy.
Researchers propose a novel theory of aging that suggests cell competition is a key factor in the process. The selective destruction theory (SDT) proposes a mechanism of aging that is independent of accumulating damage and consistent with epigenetic rejuvenation.
Dendritic cells have been found to directly kill T cells lacking CD47, providing a new insight into the immune system's ability to distinguish self from non-self. This discovery has potential implications for cancer treatment and raises questions about the therapeutic application of this novel mechanism.
Researchers have uncovered a novel mechanism of cell death regulation, shedding light on its significance during conditions such as SARS-CoV infection and skin injury. The study reveals that the cleavage of cFLIP restrains cell death during viral infection and tissue injury, favoring tissue repair.
Researchers discovered that Nerofe and Doxorubicin can downregulate KRAS signaling, leading to enhanced apoptosis in colorectal cancer cells. The combination also activates the immune system against tumor cells, increasing immunostimulatory cytokines and recruiting NK cells and M1 macrophages.
Researchers at Helmholtz Munich discovered that DHODH inhibitors sensitize cancer cells to ferroptosis by inhibiting ferroptosis suppressor protein-1 (FSP1), not DHODH itself. This finding confirms the crucial role of FSP1 in ferroptosis surveillance and opens up new avenues for developing effective cancer therapies.
Researchers investigate MCL-1i-induced Mcl-1 protein accumulation and its implications in B-cell malignancies. The study reveals a complex mechanism contributing to MCL-1 protein stability upon treatment with MCL-1 inhibitors.
Researchers at UCalgary have found that Leishmania parasites exploit immune cells by targeting receptors to gain access and resist elimination, leading to stalled apoptosis and hindered vaccination efforts.
Researchers from St. Jude Children's Research Hospital discovered NLRP12 to be the key molecule responsible for inducing inflammatory cell death and pathology in response to heme combined with other cellular damage or infection. This finding provides a new potential drug target to prevent morbidity in certain illnesses.
Researchers found that necroptosis promotes metastasis in breast cancer models, and blocking it leads to inhibition of metastasis. Necroptosis may be a key factor in tumor progression, and targeting its regulators could be critical for mitigating metastasis.
Researchers have discovered a link between iron redox and Alzheimer's disease, which could lead to the development of new drugs to treat the condition. The new imaging technique allows for the simultaneous detection of two forms of iron in cells and tissue, providing insights into its role in destroying brain cells.
Researchers have discovered that Shigella bacteria can infect humans but not mice due to differences in the shape of a key protein, gasdermin-B. The protein has six different forms, and some isoforms cause cell death while others do not, explaining why Shigella is unable to infect mice.
Tumour cells exhibit an innate randomness in their ability to respond to chemotherapy, which can lead to resistance. Researchers identified a marker for resistance and propose combining chemotherapy with drugs targeting this 'noise' to improve treatment outcomes.
Scientists at Ben-Gurion University have discovered a groundbreaking treatment approach targeting the mitochondrial gatekeeper VDAC1 for Alzheimer's disease. The new therapy, VBIT-4, demonstrates significant improvement in mouse models, preventing cell death and neuroinflammation while promoting healthy neuron growth.
Pusan National University researchers have identified a novel gene, SURF4, that regulates cell death and differentiation in acute myeloid leukemia (AML). The study found that suppressing SURF4 expression increases cell differentiation, cell death, and accumulation of ROS, leading to arrested tumor growth in mice.
Researchers found that UV nail polish dryers cause cell death, mitochondrial damage, and DNA mutations, leading to cancer-causing effects. Chronic use of these devices poses a significant public health risk.
Researchers developed a FRET-based biosensor SMART to visualize necroptosis in living mice, enabling monitoring of this form of regulated cell death in various pathological models. The study successfully characterized necroptosis in vivo using transgenic mice with the FRET biosensor.
G-Quadruplex DNA structures play a crucial role in regulating genes and cell processes, but their visualization is challenging due to the dynamic nature of double standard DNA. Fluorescence-active small molecule probes have emerged as a real-time visualization method, enabling researchers to detect G-quadruplexes with high selectivity.
Researchers from the Salk Institute have found that deteriorating neurons from people with Alzheimer's disease undergo a late-life stress process called senescence, leading to brain inflammation and neurodegeneration. By targeting these senescent cells with therapeutics, scientists hope to prevent or treat Alzheimer's disease.
Researchers at the University of Houston have developed a protocol to reprogram human heart cells into specialized cells that conduct electricity, enabling rhythmic heartbeat and repair diseased hearts. The discovery could lead to improved cardiac function and new pharmacological therapies for heart diseases.
Researchers at Goethe University Frankfurt found that dying colon cancer cells release ATP to neighboring tumor cells, activating a survival signaling pathway. Interrupting this communication can significantly increase the effectiveness of chemotherapy against resistant tumors.
Researchers have discovered that mutations in mitochondrial-related genes can trigger hyperinflammation, leading to diseases such as Crohn's disease and tuberculosis. The study found that these mutations lead to a new type of cell death called necroptosis, which causes an aggressive inflammatory immune response.
Researchers have found that delivering a cellular metabolite via tiny particles called nanoliposomes can augment the beneficial effects of certain anti-leukemia drugs in models of acute myeloid leukemia. The study also uncovered several mechanisms behind these effects.
A mutated zebrafish eye provides a glimpse into the role of banp in preventing cell death and regulating the cell cycle. The study found that banp promotes the expression of 31 genes involved in DNA repair, tumor suppression, and cell duplication.
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.
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.
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 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.
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.
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.
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.