All articles tagged with #cell death
The study investigates how UBA1 mutations in VEXAS syndrome lead to inflammation and myeloid cell bias, revealing mechanisms involving aberrant cell death and ubiquitin pathway defects, and suggesting potential therapeutic targets.
Scientists are studying 'death fold' proteins that regulate cell self-destruction to develop treatments for diseases like Alzheimer's and cancer, aiming to control when cells die or survive.
The study reveals that STING can induce ZBP1-mediated necroptosis independently of TNFR1 and FADD, highlighting a novel pathway in cell death and immune response regulation.
New research suggests that controlling or pausing necrosis, a chaotic form of cell death linked to inflammation and tissue damage, could be key to slowing or reversing aging and treating chronic diseases, with implications for space travel and organ health.
Scientists are exploring a novel approach to combat aging by targeting necrosis, an uncontrolled form of cell death, which may help prevent tissue damage and age-related diseases, potentially extending healthspan and improving outcomes for conditions like kidney, heart, and brain diseases, as well as aiding space exploration health strategies.
A new study suggests that uncontrolled cell death called necrosis may be a key driver of aging and many diseases, including cancer, heart disease, and neurodegeneration. Controlling necrosis could revolutionize treatments by preventing tissue damage and disease progression, although targeting it remains challenging due to its complex mechanisms.
Cell death, often seen as a loss, is crucial for life, playing significant roles in development, disease prevention, and evolution. Cellular biologist Shai Shaham discusses with Steven Strogatz the various forms of cell death, such as apoptosis and necrosis, and their importance in biological systems. Understanding these processes can aid in medical advancements, particularly in treating diseases where cell death is either excessive, like in neurodegenerative diseases, or insufficient, as in cancer.
A study reveals that mature oligodendrocytes, crucial for brain function and myelin production, have an extended death process, surviving up to 45 days post-trauma, compared to the rapid demise of younger cells within 24 hours. This discovery suggests potential age-specific treatment strategies for aging-related damage and neurodegenerative diseases like multiple sclerosis, challenging the current one-size-fits-all approach. Understanding the prolonged cell death process in mature oligodendrocytes could lead to better management of conditions involving myelin damage.
Researchers at Columbia University have identified a rare lipid, diPUFA phospholipid, as a crucial factor in promoting ferroptosis, a unique form of cell death. This discovery has significant implications for treating neurodegenerative diseases and cancer, as it opens new avenues for either preventing or inducing cell death. The interdisciplinary research involved the Department of Biological Sciences, Department of Chemistry, and the Columbia University Irving Medical Center, and the findings deepen our understanding of ferroptosis and its potential for controlling cell death.
Researchers have discovered that 7-dehydrocholesterol (7-DHC), a molecule used to make cholesterol, acts as a defense against ferroptosis, a form of regulated cell death. This finding could lead to new treatments for cancer and other clinical conditions, shedding light on the underpinnings of cell protection mechanisms.
A study has identified 7-dehydrocholesterol as a natural inhibitor of ferroptosis, a form of cell death driven by lipid peroxidation. The research sheds light on the role of 7-dehydrocholesterol-derived oxysterols in regulating ferroptosis sensitivity and provides insights into the mechanisms of this type of cell death. The data and materials supporting the findings are available in the main text, figures, and extended data figures, as well as in a repository for (epi)lipidomics experiments.
A study conducted by the University of Pennsylvania has found that injecting the local anesthetic lidocaine near the site of head and throat tumors can activate bitter taste receptors (T2Rs) in cancer cells, leading to cellular death. Lidocaine was already suspected to be beneficial to cancer patients, but this study provides a better understanding of how it works. The findings could potentially improve treatment options for head and neck cancer patients and pave the way for clinical trials combining lidocaine with standard cancer therapies.
Lidocaine, a commonly used local anesthetic, has been found to have anticancer properties by activating the T2R14 taste receptor, which is highly expressed in various cancer cells. Researchers at the University of Pennsylvania discovered that lidocaine triggers a cascade of cellular signals that lead to controlled cell death. This finding offers hope for improving treatment options for head and neck cancer, which has a high mortality rate. Lidocaine could potentially be injected near accessible oral tumors and may also benefit patients with other forms of cancer. The study opens the possibility of repurposing other drugs that activate the T2R14 receptor for cancer treatment. Clinical trials are hoped to be conducted to explore the addition of lidocaine to standard care therapy for head and neck cancer patients.
Scientists at UC Davis in California have identified a "switch" that can activate the death of cancer cells, potentially revolutionizing cancer treatment. The discovery allows for targeted killing of cancer cells without harming healthy cells. The research has been successful in labs but has not yet been tested on animals or humans. The treatment has shown effectiveness in liquid cancers but not solid tumors. The major drawback is the estimated cost of $500,000.
Researchers from the UC Davis Comprehensive Cancer Center have identified an epitope on the CD95 cell receptor, known as Fas, that can trigger the death of cancer cells. This discovery could lead to the development of new therapeutics to effectively target and kill cancer cells. By developing antibodies that selectively bind to and activate Fas in solid tumors, researchers hope to spark cell death and potentially enhance the efficacy of current cancer treatments. Additionally, the identification of this epitope could serve as a biomarker for the effectiveness of CAR T-cell immune therapy.