Articles tagged with Fibrosis
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.
The American College of Chest Physicians journal features cutting-edge original research on various chest medicine topics, including asthma, COPD, critical care, and sleep. The March issue includes a special series on nontuberculous mycobacterial pulmonary disease, offering insights into clinical epidemiology, risk factors, and diagnosis.
A biodegradable nanoparticle has shown promise in reducing skin and lung scarring in mice with scleroderma. The treatment targets specific immune cells responsible for the disease's chronic inflammation and scarring.
Researchers found a relationship between regionalized fibrosis in the left ventricle and mitral valve prolapse disease, suggesting potential benefits from earlier surgical intervention. Advanced fibrosis could be added to traditional markers for mitral valve repair.
A new study suggests that incomplete lung cell repair may contribute to the development of chronic fibrotic lung disease in COVID-19 and non-COVID patients. The research proposes novel therapies to promote healthy regeneration and prevent scarring.
A new pathway has been discovered to explain how excessive alcohol consumption damages the liver, specifically through mitochondrial dysfunction. By targeting an enzyme called MATα1, researchers believe they can develop a new treatment for people suffering from alcohol-associated liver disease.
Researchers found that higher monocyte counts are linked to early signs of injury and scarring on lung imaging among community-dwelling adults. This suggests that hyperactive monocytes may contribute to lung injury at the early stages of interstitial lung disease.
Researchers at Brown University have developed a new laboratory test model to investigate fibrosis treatments without the use of animals. The model uses human cells and replicates not only the structure of human tissue but also its mechanics, enabling scientists to study the underlying mechanisms of fibrosis and test potential treatments.
Researchers at MUSC identified a potent antifibrotic peptide that reverses scarring in human and mouse tissues by activating an antifibrotic pathway. The E4 peptide has the potential to treat various diseases, including heart disease, lung fibrosis, liver cirrhosis, and chronic kidney disease.
Research from MUSC suggests that physicians should be cautious when using laboratory tests to diagnose alcoholic cirrhosis due to false negative results. Patients with advanced liver disease often show subtle signs and symptoms in the early stages of cirrhosis.
Researchers found that macrophages play a central role in COVID-19-related respiratory failure, leading to fibroproliferative ARDS and prolonged ventilation. Extensive tissue damage and scar tissue formation are characteristic of severe lung failure.
Pathologists have discovered that some patients with lingering COVID-19 symptoms may have underlying chronic lung disease prior to their infection. This finding suggests that clinicians should carefully consider alternative explanations for respiratory symptoms beyond long COVID.
Researchers found that candesartan reduces accumulation of extracellular matrix proteins and normalizes blood flow in mice with hereditary cerebral small vessel disease. The study suggests a potential new treatment avenue for age-related cerebral arteriopathy.
Researchers have developed a 3D cell culturing platform that allows study of lung fibroblasts and their microenvironment, enabling measurement of cell behaviors and microenvironment changes involved in IPF disease progression. The system's versatility enables personalized medicine and potential applications in studying other diseases.
Researchers at Tokyo Medical and Dental University discovered a genetic variant associated with a poorer prognosis of chronic hypersensitivity pneumonitis. The variant, rs5743899, was linked to increased immune activation and fibrosis, leading to reduced lung function in patients.
Researchers aim to reverse tissue damage and scar buildup in lungs affected by Idiopathic Pulmonary Fibrosis (IPF) using a protein domain. The team hopes to identify therapeutic agents that can be used to treat the disease, which affects 100,000 Americans annually.
Scientists discovered an important protective response in the heart that can prevent excessive scarring after a heart attack. The study found that this reactive response can limit cardiac fibrosis by preventing oxidant build-up in heart cells, potentially leading to new therapies to repair scarring damage.
Researchers have identified a novel estrogen compound that provides benefits similar to hormone replacement therapy but without the risk factors associated with it. The compound has been shown to reduce excess lipid deposition in the liver and prevent the progression of fibrosis, which can lead to liver failure and metabolic problems.
Researchers found that hepatitis C treatment reduces the activity of proteins involved in cirrhosis, potentially indicating an early sign of liver recovery. The study suggests a possible pathway toward healing scarred liver tissue after virus elimination.
Researchers identified specific mesenchymal stromal cells within the bronchovascular bundle of lungs that play a crucial role in creating scarring through interaction with epithelial cells. These cells are thought to be triggered by immune cell attacks, leading to fibrotic scarring and rejection.
Researchers at USask discovered excessive sodium absorption in small airways of CF patients, providing new insights into the disease. The study's findings have the potential to improve life for people with CF who cannot benefit from existing medications.
A study led by Vanderbilt University Medical Center aims to identify the origins of pulmonary fibrosis in an at-risk patient population. The research, funded by Three Lakes Foundation, focuses on single-cell tissue samples from pre-symptomatic individuals to investigate the beginning of early interstitial lung disease.
A prospective study found that liver stiffness measurements obtained by shear-wave elastography decreased significantly after image-guided intervention for chronic Budd-Chiari syndrome in children. Disease recurrence was typically associated with an increase in liver stiffness measurements compared to prior assessments.
A new study found that every extra 1cm in waist circumference increases the odds of advanced fibrosis by 5% in people with type 2 diabetes. Advanced fibrosis is a late stage of non-alcoholic fatty liver disease (NAFLD), which can lead to serious liver damage.
A serum biomarker, polyubiquitinated phosphatase and tensin homolog (PTEN), was associated with a four-fold higher risk of kidney function decline. This modified form of PTEN was linked to severity of lesions in kidney structure, indicating early manifestations of diabetic kidney disease.
Researchers reverse lung fibrosis in a mouse model using Bcl-2 inhibitor ABT-199, suggesting a novel therapeutic target to treat idiopathic pulmonary fibrosis. The study finds that monocyte-derived macrophages play a key role in fibrosis progression and that targeting the Cpt1a-Bcl-2 interaction modulates apoptosis resistance.
Researchers at Skoltech have discovered structures called apical bulkheads in liver cells that are responsible for the narrow shape of bile canaliculi. The discovery reveals a key role for the Rab35 protein in regulating hepatocyte lumina formation and suggests potential avenues for medical applications in fatty liver disease and fibrosis
A subset of fibroblasts in lungs of people with idiopathic pulmonary fibrosis (IPF) produce a protein called meflin, which protects against cell aging and fibrosis. Further research could lead to novel therapies for lung fibrosis.
Non-alcoholic fatty liver disease affects 25% of the global population, leading to inflammation and fibrosis. Researchers discovered that hepatocyte reprogramming is controlled by molecular switches, resulting in dysfunction.
Researchers at University of California San Diego have found that immunotoxins targeting mesothelin can prevent liver cells from producing collagen, a precursor to fibrosis and cirrhosis. In mouse models, these antibodies killed 60-100% of human mesothelin-producing cells, reducing collagen deposition.
Researchers at Gladstone Institutes have discovered a master switch for fibrosis in the heart, which they believe could be used to treat and prevent heart failure. The study suggests that blocking this gene, MEOX1, could prevent fibrosis in other organs as well.
Researchers developed a new PET/CT radiotracer that targets activated fibroblasts in lungs, enabling direct imaging of pulmonary fibrosis. The study showed promising results, suggesting the radiotracer's potential to reduce lung biopsies and improve disease management.
Researchers at the University of Illinois Chicago have developed a microgel coating that can optimize cell-based therapy for pulmonary fibrosis. The coating boosts the therapeutic potential of donor cells by degrading scar tissue and promoting healthy lung tissue regeneration.
Fibroblasts, the cells responsible for extracellular matrices, become diseased in fibrosis. Researchers create 3D hydrogels that mimic living tissue to study fibrosis progression and epigenetic responses.
A nationwide clinical trial found no benefit from antibiotics in preventing hospitalization or death for patients with idiopathic pulmonary fibrosis. The study collected biological samples that will advance the understanding and treatment of the disease.
Researchers at UCSF have found a way to stimulate the natural surveillance system of immune cells to eliminate senescent cells, which contribute to aging and chronic diseases. This discovery offers an alternative to existing senolytic therapies and may lead to new treatments for age-related chronic diseases.
Researchers from Skoltech, Italy, discovered a new axis for preventing liver fibrosis by targeting the GILZ protein. The study used mice models and verified findings with human clinical data, suggesting that controlling the signaling pathway involving GILZ could lead to treating inflammatory liver diseases.
Researchers at UC Irvine discover the interaction between stromal progenitors and ILC2s that promotes muscle eosinophilia and fibrosis-associated gene expression. This finding could lead to the development of new treatments for Duchenne muscular dystrophy, a fatal muscle disease.
Researchers highlight the importance of myocardial fibrosis in HCM diagnosis and treatment, citing gene mutation and abnormal energy metabolism as contributing factors. The use of magnetic resonance imaging is also discussed as a diagnostic tool for fibrosis.
Researchers found a link between citrullinated vimentin, produced by lung macrophages in response to environmental pollutants, and the development of lung fibrosis. The study suggests that targeting PAD2 enzyme could attenuate cadmium/carbon black-induced fibrosis.
Renal fibrosis, a leading cause of kidney failure, has been linked to telomere shortening. Researchers found that short telomeres exacerbate epithelial-to-mesenchymal transition, promoting pathological scarring of kidney tissue. They propose treating renal fibrosis by lengthening telomeres and restoring normal gene expression.
Researchers investigate using a cell-signaling chemokine from cats to treat human kidney fibrosis and slow disease progression. The study suggests that intra-renal injection of CXCL12 may be a potential therapy for early kidney disease, offering new hope for millions with the condition.
Researchers have identified a new molecular target, MDM4, that could potentially treat idiopathic pulmonary fibrosis (IPF) by initiating a genetic program to remove scar tissue from the lungs. Targeting this protein may prevent respiratory failure and improve treatment options for patients with IPF.
Researchers found that conventional diagnostic methods for liver fibrosis do not accurately track the disease in patients who underwent Fontan surgery. The study revealed a unique regional development of fibrosis, which was not observed with hepatitis C and B, highlighting the need for new biomarkers and imaging techniques.
Advanced liver fibrosis worsens cancer-specific and overall survival in iCCA patients, regardless of surgical resection. Patients with advanced fibrosis are at increased risk of mortality across follow-up periods.
A study published in the American Journal of Roentgenology found that multiparametric CT findings can distinguish patients with high-risk NAFLD, characterized by advanced fibrosis or cirrhosis. However, the presence of nonalcoholic steatohepatitis (NASH) remains elusive on CT.
Researchers will develop a human, three-dimensional model system for IPF using induced pluripotent stem cells to better understand its mechanisms. The study aims to provide insights into the development of IPF and potential new treatments.
A study published in Cell Reports Medicine found a link between autoantibodies and lung fibrosis progression in systemic sclerosis patients. The researchers discovered that osteopontin, a protein previously implicated in fibrosis, may be responsible for triggering lung scarring.
Research reveals a direct relationship between insulin resistance and severe lung inflammation and scarring in people with pre-diabetes or diabetes. High ozone exposure may exacerbate pulmonary fibrosis, particularly in individuals with poorly controlled diabetes.
A new study has found that short telomeres may contribute to the cause of idiopathic pulmonary fibrosis (IPF), a devastating lung disease affecting thousands in the UK. The research also suggests that reducing stress and increasing exercise may help prevent or treat IPF.
Lung tissue analysis reveals MBD2 as a promising target for treating lung fibrosis, which is characterized by overexpression of this epigenetic regulator in areas occupied by macrophages. Inhibiting MBD2 may prove to be a safe way to treat the chronic and irreversible disease.
A new diagnostic tool has been developed by MIT engineers to detect both fatty liver disease and fibrosis, which can lead to liver failure. The sensor uses nuclear magnetic resonance (NMR) technology to measure water diffusion in tissue, revealing the presence of fatty or scarred tissue with high accuracy.
A new study has identified fifty protein fragments, termed peptides, in the urine of patients with liver fibrosis, which could be used to develop a diagnostic urine test for the condition. The research team found that these peptides were accurately detected in 84.2% of liver fibrosis patients and 82.4% of those without the condition.
Researchers at MUSC discover lysyl oxidase plays key roles in promoting fibrosis in scleroderma, and its levels can be used to monitor treatment response. The findings suggest LOX could be a promising biomarker for assessing fibrosis progression or regression.
Researchers have developed two novel targeted therapies to slow down or stop fibrosis progression in people with idiopathic pulmonary fibrosis (IPF). These treatments aim to deliver potent drugs specifically to diseased cells, minimizing harm to healthy ones. The therapies will soon enter human clinical trials.
A study of nearly 3,000 middle-aged Framingham Heart Study participants found that approximately nine percent had clinically significant liver fibrosis. Liver stiffness correlates with the degree of scarring, which is associated with more adverse cardiometabolic risk factors.
Scientists have developed a new method to study glycans and their interactions with proteins, expanding our understanding of liver disease and the immune system. Galectin-3, a glycan-binding protein, was found to interact with hundreds of receptors in live liver stellate cells and immune cells.
Researchers developed a novel ultrasound technique that quantifies lung scarring and detects lung fluid in rats, showing promise for assessing pulmonary fibrosis and edema. The non-invasive method could reduce costs and improve patient care by providing accurate, measurable assessments of lung health.
Researchers at La Jolla Institute for Immunology report that protein TL1A drives fibrosis in several mouse models, triggering tissue remodeling and making it harder for lungs and airways to function normally. This discovery suggests potential targets for therapeutics aimed at reducing fibrosis and tissue remodeling.
Researchers developed a 3D bioengineered model of lung tissue that showed drugs effective in Petri dish tests did not work in patients, highlighting the need to target other aspects of pulmonary fibrosis. The study used tissue engineering and mechanical cues to understand how fibroblasts drive disease progression.