Articles tagged with Inflammatory Signaling
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Researchers have discovered a new role for VWF in regulating immune responses at sites of blood vessel injury, leading to potential treatment options for inflammatory and blood clotting disorders. The study found that VWF plays a key role in repairing damaged blood vessels, which could help prevent heavy bleeding and blood clots.
Researchers at the University of Bonn have identified a new signaling pathway that triggers inflammatory responses in the skin after UV damage. This pathway involves the activation of p38 molecularly modifying NLRP1, a critical switch for inflammation, and initiates the assembly of inflammasomes.
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.
Two studies found that cigarette smoke and e-cigarette vapor have similar cardiovascular effects due to airway irritation. This irritation can lead to vascular damage and impaired blood vessel function. The research suggests that dual product use may be worse than single product use, highlighting the need for stricter regulations.
A new strategy for treating rheumatoid arthritis has been proposed, integrating small interfering RNAs and Prussian blue nanoparticles to silence proinflammatory cytokines and scavenge reactive oxygen species. The approach was tested in a mouse model, showing improved therapeutic efficacy and real-time monitoring capabilities.
Researchers at Weill Cornell Medicine found that gut pain-sensing neurons regulate the microbial community in the intestines, boosting beneficial microbes to protect against inflammation. The study suggests that targeting these neurons could lead to new anti-inflammatory treatments for IBD and other disorders.
The study found that a combination of NOX1, loss of function, and TNF leads to an abnormal increase in microfold cells, driving increased recruitment of immune cells. Reversing the defect with reactive oxygen species restored healthy gut balance. Further studies on reactive oxygen species-stem cell modulation therapy are proposed.
Researchers have discovered that neurons with double-stranded breaks (DSBs) in their DNA actively trigger an inflammatory response, which is mediated by the activation of the NFkappaB transcription factor. This process elicits an immune response from microglia, leading to synaptic loss and cognitive function impairment.
A study by Kumamoto University researchers found that a defective isoform of the SIGIRR gene activates an inflammatory pathway associated with cystic fibrosis. This defect leads to decreased expression and function of anti-inflammatory molecules, resulting in severe inflammation.
Researchers at Michigan Medicine have discovered a molecular mechanism that drives the disease-causing effects of the most common genetic risk factor for lupus. The study suggests that targeting this new pathway could lead to the development of safe and effective treatments for SLE, an autoimmune disease that affects millions worldwide.
University of Cincinnati researchers are studying whether targeting an inflammation pathway can improve patient results for soldiers with burn injuries combined with traumatic brain injuries. The research focuses on a specific protein that causes inflammation, which can lead to complications such as anemia and death.
Researchers identified toll-like receptor (TLR) signaling as a novel pathway regulating GLI3 expression, which plays a role in inflammatory cytokine production and cancer. They found that IRF3 directly binds to the GLI3 promoter region, increasing its expression upon TLR4 stimulation.
Researchers found that DNMT3A and TET2 genes directly activate expression of a gene involved in mitochondrial inflammatory pathways. This activation leads to increased inflammation, which may exacerbate plaque buildup in atherosclerosis. Blocking these pathways could form the basis for new treatments.
A team of researchers found that two SARS-CoV-2 proteins, NSP6 and ORF7a, are essential for activating the NF-κB pathway, leading to elevated cytokine levels. The study suggests that targeting this pathway may offer a strategy to stop the virus.
Astrocytes in the thalamus play a key role in susceptibility to seizures after brain injuries. Targeting a specific protein, GAT3, in these cells may prevent long-term damage.
A new study from Oregon State University suggests that the gelatin in Pacific whiting skin has anti-aging properties, preventing wrinkles caused by ultraviolet radiation. The researchers found a positive response in a human cell model system, providing evidence for further research.
Researchers identified immune endothelial cells promoting inflammation and developmental endothelial cells supporting cell development, regeneration, and proliferation. The study's findings may lead to targeted treatments for lung infections and acute respiratory distress syndrome.
Scientists at CNIC discovered a complex network between liver tissue connections that allows the liver to regulate body temperature. The secretion of IL-12 by liver-infiltrating macrophages blocks FGF21 production, reducing heat generation by brown fat in mice.
Researchers at Karolinska Institutet discovered that electrical stimulation of the vagus nerve promotes healing in acute inflammation by shifting the balance between inflammatory and anti-inflammatory molecules. This finding opens new avenues for treating inflammatory diseases, including autoimmune and cardiovascular conditions.
A new review highlights the risks of fatty liver disease caused by metabolic dysfunction, characterized by fat accumulation in liver cells and oxidative stress. The progression of the disease can lead to inflammation, fibrosis, and cirrhosis with a high risk of hepatocellular carcinoma.
A Johns Hopkins Medicine study found that a protein called STING responds to clean-up signals in brain cells damaged by Parkinson’s disease by creating a cycle of inflammation that accelerates the disease’s progression. In mice with deactivated STING proteins, there was less microglial activity and brain cell death.
Researchers at Hokkaido University discovered that ATP secreted from sensory neuron-interneuron crosstalk triggers inflammation spread across joints, acting as a neurotransmitter and inflammation enhancer. Blocking this pathway prevents the spread of inflammation.
Researchers found that normal-appearing lupus skin contains the same inflammatory signals as skin with rashes, suggesting a primed state for inflammation. The study's findings provide new insights into how UV light triggers rashes in lupus patients and highlight the potential for precision medicine in treating the disease.
A study has identified disease mechanisms in children with severe COVID-19, including blood clotting and immune protein pathways. The research found specific proteins involved in multisystem inflammatory syndrome and acute respiratory distress syndrome, which are major potential outcomes of severe COVID-19.
A study published in Brain reveals a dedicated neural circuit responsible for post-sepsis anxiety and depression. The researchers identified a potential pharmacological treatment by silencing the amygdala circuit during sepsis, reducing the risk of developing anxiety disorders.
A study led by Boston Children's Hospital researchers found that COVID-19 causes severe inflammation through infected immune cells. Antibodies developed during infection may sometimes contribute to inflammation.
A study published in The Lancet Respiratory Medicine found that astegolimab reduced exacerbation rates by 22% and improved quality of life in patients with moderate-to-severe COPD. Benefits were seen in those with specific inflammatory signals and genetic markers.
Researchers at LSU Health New Orleans and Karolinska Institutet found that intranasal application of pro-resolving lipid mediators arrested memory loss and brain degeneration in an experimental Alzheimer's model. This discovery opens up new possibilities for therapeutic interventions for Alzheimer's disease.
Dixit's work on programmed cell death and inflammation has led to therapies for autoimmune disorders and rheumatoid arthritis. The Vilcek Foundation recognizes his contributions as an immigrant scientist in the US.
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 from the University of Pennsylvania and Oak Ridge National Laboratory have identified a cascade of inflammatory signaling that precedes skin ulcers in atopic dermatitis. A mouse model lacking an activator of NF-kB signaling led to the development of skin lesions, shedding light on the early stages of the condition.
Researchers found that prunes' phenolic compounds and dietary fiber content may alter gut microbiome, decreasing inflammatory markers and improving bone turnover. Clinical trials showed promising effects of prune consumption on bone health outcomes in postmenopausal women.
A UC Davis Health study found that taking bile acids or treatments regulating their production levels can help control psoriasis inflammation. Bile acids inhibited skin inflammation by stopping immune T cells from producing proinflammatory protein IL-17A and blocking immune cell movement to the site.
Scientists have found evidence that carnosic acid in rosemary can block SARS-CoV-2 infection and reduce inflammation. The compound has been shown to inhibit the powerful inflammatory pathway active in severe COVID-19 and other diseases.
Researchers discovered that wound macrophages undergo different metabolic programs to coordinate tissue repair, including the use of reactive oxygen radicals for blood vessel growth. Macrophages also utilize a different type of mitochondrial exchange for anti-inflammatory and reparative functions in late-stage wound healing.
Researchers from Tokyo Medical and Dental University found that PQBP1 interacts with Tau protein to drive an immune response in the brain. The study reveals a mechanism of inflammation that functions in both viral infection and neurodegenerative disease.
A study by Tokyo University of Science researchers identifies a novel regulatory axis targeting dendritic cell activity, suppressing autoimmune disease symptoms and bone loss. They discovered DCIR binds to glycoproteins on macrophages and osteoclasts, reducing inflammation and immune responses.
A new study from Keck School of Medicine of USC shows that vaping is associated with dysregulation of mitochondrial genes and immune response genes, similar to smoking. The research found that over 80% of gene dysregulation in vapers correlated with the intensity and duration of current vaping.
Researchers discovered that altering macrophage metabolism helps prevent overloading and resolves inflammation by protecting mitochondria from strain. This process enables efficient removal of damaged cells, a key factor in resolving inflammation.
Itepekimab, a novel monoclonal antibody, has been found to be safe and effective in treating moderate-to-severe asthma. In a phase 2 trial, it significantly improved lung function and reduced asthma control events compared to placebo.
Researchers from the University of Tsukuba found that blocking CD300a enhances efferocytosis and ameliorates neuronal deficits after ischemic stroke. This process involves the removal of damaged cells in the brain, reducing inflammation and neurological impairment.
A pre-clinical study by University of Illinois Chicago researchers shows that a drug targeting specific immune pathways can prevent lung damage and death in mice infected with the SARS-CoV-2 virus. The study suggests targeted treatments may be more suitable for COVID-19 patients than broad immune suppressants.
Researchers comprehensively review T-cell responses to respiratory viral infections and chronic obstructive pulmonary disease (COPD), highlighting key characteristics of peptide-reactive T-cells. The review aims to improve understanding of the underlying mechanisms, leading to more effective immune protection and treatment methods.
Researchers discovered a combination of two drugs can reduce inflammation following chemotherapy, preventing metastasis in pancreatic and liver cancer. The treatment targets the sEH and EP4 pathways, modulating inflammation to resolve cytokine storms.
A study by Cincinnati Children's Hospital Medical Center has identified a common biological response platform that could help alleviate allergic inflammation. The research suggests that inhibiting this pathway may provide a unique opportunity to counteract type 2 immunity and reduce allergic reactions.
Researchers found that the gene TCF-1 regulates specific Treg cells, leading to more severe and inflammatory colon cancers. Without TCF-1, these cells become activated and gain a gut-homing feature, resulting in harsher cancer outcomes.
A new study reveals a 'weak point' in a type of gut bacteria that causes intestinal inflammation in patients with Crohn's disease. The researchers found that interfering with the bacteria's process relieved gut inflammation in a mouse model of Crohn's disease.
Scientists at UT Southwestern Medical Center have discovered a type of cell responsible for triggering chronic inflammation in fat tissue. The study found that these cells, called fibro-inflammatory progenitors (FIPs), produce signals that encourage inflammation when exposed to high-fat diets.
Dr. Tim Denning receives a $1.67 million grant to study the IL-36/IL-36 receptor axis in gut immunity and its potential therapeutic value for treating inflammatory bowel disease.
A research team at Trinity College Dublin has discovered that PKM2 is a central 'on' switch for immune cells involved in psoriasis and multiple sclerosis. Interfering with PKM2 blocks these cells and limits inflammation, offering new potential treatments for these diseases.
Researchers at Michigan Medicine discovered a previously unrecognized link between inflammation and deep vein thrombosis, finding that blocking a key inflammatory molecule reduced clot formation in mice.
Researchers found that neurosteroids inhibit Toll-like receptor 4 signaling activation, preventing pro-inflammatory protein production and cytokine creation. This discovery provides a new target for treating brain diseases, including alcoholism, depression, and posttraumatic stress disorders.
Researchers at the Buck Institute have identified a novel molecular mechanism that orchestrates harmful inflammatory signaling in glial cells, contributing to Parkinson's disease pathology. Blocking Furin 1, a catalytic protein, in dopaminergic neurons reduces toxic cross-talk and protects neurons from degeneration.
Researcher Phillip Owens aims to find better treatments for heart disease by studying PAR2 receptor's role in atherosclerosis. High cholesterol significantly increases risk of arterial thrombosis through modification of coagulation proteins.
Researchers found that activating inflammatory signaling in heart cells can lead to abnormal electrical patterns similar to those observed in atrial fibrillation. This suggests a potential new target for therapies aiming to treat the condition.
Weizmann Institute of Science researchers found a natural defense mechanism that prompts the body to alleviate intestinal inflammation. Boosting signals in certain cells, such as those making up the inner lining of the gut, may help treat inflammatory bowel diseases and potentially even colon cancer.
Scientists have discovered key regulators that control the inflammatory response in chronic diseases such as Crohn's disease and multiple sclerosis. The NOD2 pathway plays a critical role in detecting bacterial invaders, but faults in its regulation can lead to uncontrolled inflammation.
Researchers discovered that innate immune system's DNA-sensing mechanism controls cellular senescence, promoting the secretion of inflammation-mediating proteins. This process plays a role in various contexts of senescence, including oxidative stress, oncogene signaling, and irradiation.
Researchers discovered that targeting the TGF-β1 pathway can reduce pro-inflammatory signals and improve motor function in mice after intracerebral hemorrhage. In human patients, higher levels of TGF-β1 within the first 3 days following stroke predicted better outcomes three months into recovery.
Researchers found that an extract from house dust mites triggers different responses depending on the age of the person, with leukotrienes playing a key role in adults. The study suggests that cortisone therapy may not be effective against this type of allergy and that targeted therapies could be more effective.