Articles tagged with 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.
Scientists discovered that type-1 innate lymphoid cells (ILC1) promote tissue repair in the gut, but when dysregulated can contribute to IBD co-morbidities such as cancer and fibrosis. This finding has important implications for treating patients with inflammatory bowel diseases.
A pilot study found that assessing liver fibrosis in people with type 2 diabetes could identify large numbers of previously undiscovered cases of advanced liver disease, increasing diagnosis rates 5-fold. The study also discovered that over half of patients diagnosed with significant fibrosis had normal ALT levels.
Researchers from Kanazawa University found that IL-17A triggers cellular changes in the peritoneum, leading to stromal fibrosis in gastric cancer patients. The study suggests that suppressing mast cell degranulation may be a promising treatment strategy for patients with peritoneal dissemination.
A study published in JCI Insight has identified a potential treatment for non-alcoholic fatty liver disease (NAFLD), with tesamorelin reducing liver fat and fibrosis progression. The drug appears to increase expression of genes associated with burning of fat in the mitochondria, which may prevent fibrosis.
Researchers at CNIO develop effective therapy for mice with age-related pulmonary fibrosis, activating telomerase production to prevent disease development. The treatment, a gene therapy, also successfully reversed fibrosis in mice without genetic alterations.
A pre-clinical study led by Cincinnati Children's Hospital demonstrates that barasertib reverses fibroblast activation, stopping dangerous scar tissue build-up in lungs of IPF patients. The drug targets AURKB activity, slowing disease progress and improving lung function.
Researchers at IRB Barcelona have been awarded an ERC grant to develop new medications targeting senescent cells, which contribute to fibrotic diseases. The goal is to create senolytics that selectively eliminate damaged cells, potentially preventing age-related diseases.
Researchers at Okayama University developed a novel 3D cell culture model that accurately replicates the fibrotic components of pancreatic cancer. The model allows for the tuning of fibrosis levels, enabling a better understanding of how it hinders cancer treatment and its therapeutic ramifications.
Scientists have discovered previously unreported genetic and cellular changes in the lungs of people with pulmonary fibrosis, a devastating lung-scarring disease. The findings provide remarkable insights into the fundamental mechanisms driving disease pathology in PF and may aid the search for new ways to treat or prevent the condition.
A groundbreaking study published in Science Advances has identified five unique cell types associated with lung fibrosis, including a pro-fibrotic epithelial cell that drives the disease. The research also reveals high plasticity in lung cells, allowing them to transform into different types under certain conditions.
A novel microbiome-based diagnostic tool has been developed to quickly and inexpensively identify liver fibrosis and cirrhosis in patients. The non-invasive method analyzes patient stool samples and achieves an accuracy of over 90% in diagnosing cirrhosis, with potential implications for improving treatment outcomes.
A study by Massachusetts General Hospital researchers found that a protein called AP-2 beta induces expression of KCTD1, which triggers kidney structure differentiation. The discovery could lead to therapeutic approaches to block reactivation of beta-catenin in the adult kidney to inhibit renal fibrosis.
Researchers discover e-cigarette liquid can cause lung tissue repair process to go haywire, leading to scarring. Inhibiting a certain nicotinic receptor may help promote cell death and slow scar formation in affected individuals.
Researchers discovered that the loss of NEDD4-2 protein leads to impaired mucociliary clearance and dysregulation of the TGF? signaling pathway, contributing to pulmonary fibrosis progression. The study provides a novel animal model for IPF research, enabling further investigation of disease mechanisms and development of new treatments.
Research reveals TGF-β-driven reduction of cytoglobin (CYGB) in HSCs leads to oxidative DNA damage and liver fibrosis in NASH. CYGB has a protective effect on hepatic parenchymal cells by scavenging hydroxyl radicals.
Researchers have found a way to halt and reverse muscle fibrosis caused by overuse injuries in animal studies. The discovery uses the drug FG-3019 to block protein CCN2, which promotes connective tissue growth, leading to significant improvements in muscle strength.
A recent study published in Immunity identified the protein Rbm7 as a key player in the development of tissue fibrosis. The researchers found that Rbm7 induces cell death after tissue injury, leading to the recruitment of immune cells that form scar tissue.
Researchers at University of Illinois and Mie University discover salt-loving bacteria secret a peptide that rapidly kills lung cells, leading to acute exacerbation. The finding offers a potential new target for treating pulmonary fibrosis, a disease affecting millions worldwide.
A new technology has been used to investigate the cellular processes involved in liver fibrosis development, revealing key genes and cell types that correlate with fibrogenesis. The findings have potential applications for diagnostic tools and therapies.
Researchers found that liver fibrosis is tied to a specific type of heart failure, known as preserved ejection fraction heart failure (HFpEF), which affects people with and without HIV and hepatitis C. The study suggests that preventing liver fibrosis may be crucial in reducing the risk of HFpEF.
A new study from North Carolina State University found that lung stem cell secretions delivered via nebulizer can help repair lung injuries due to multiple types of pulmonary fibrosis in mice and rats. The treatment resulted in a nearly 50% reduction of fibrosis compared to mesenchymal stem cells counterparts.
Researchers have identified three genes linked to idiopathic pulmonary fibrosis (IPF), a devastating lung disease. The discovery provides potential targets for new drugs and may lead to improved treatments.
A team of Yale researchers has discovered a way to reverse type-2 diabetes and liver fibrosis in mice, highlighting the potential for targeting TET3 protein. The studies, published in Cell Reports and Nature Communications, also suggest that TET3 plays a role in fibrosis development and may be a key target for treatment.
Researchers at UC San Diego School of Medicine identified genetic switches that determine whether or not liver cells produce collagen, leading to a potential therapeutic target for liver fibrosis. By manipulating these transcription factors, liver fibrosis progression can be addressed.
Scientists discovered that magnetic nanoparticles can target and treat liver fibrosis by delivering drugs to the affected tissue, reducing inflammation and improving liver function. This new approach offers a potential solution for treating this fatal illness with improved patient outcomes.
A UK study found that over 20% of young adults have fatty liver disease, with those who are overweight or obese at greatest risk. The research highlights the need for improved liver health awareness and management among this age group.
A study found that people who sleep 4 hours or less double their risk of pulmonary fibrosis and those who sleep 11 hours or more triple their chance. The researchers attribute this to the body clock and suggest targeting it as a potential target for treating the disease.
Researchers propose using transient elastography as a screening method for detecting liver fibrosis in primary care. The study shows that this approach is highly cost-effective and can improve patient outcomes, with a 12% probability of cost saving.
A team led by Dr. Brigitte Gomperts developed a 'scar in a dish' model that accurately replicates progressive scarring in human organs, enabling the identification of a drug candidate that halted or reversed fibrosis in animal models.
A study suggests that monocyte-derived macrophages can induce lung fibrosis without prior alveolar epithelial cell injury. The research found increased flux through the mevalonate pathway in bronchoalveolar cells from IPF patients, which exacerbates fibrosis.
Researchers at Mayo Clinic have identified a way to slow and reverse fibrosis by targeting a dopamine receptor, which blocks the growth of scar-forming cells. The approach reversed fibrotic processes in lung and liver models, offering a new treatment concept for fibrotic diseases.
Researchers at Georgia State University have developed a protein-based contrast agent that can detect early-stage liver diseases, including liver fibrosis, with high accuracy and sensitivity. The new method uses a lower dosage of contrast metal gadolinium, reducing the risk of metal toxicity and enabling earlier diagnosis and treatment.
Researchers have identified a genetic mutation in the SFTPA1 gene that causes idiopathic pulmonary fibrosis (IPF), a progressive lung disease characterized by scar tissue buildup. Inhibiting necroptosis, a cell death pathway, could be a new therapeutic approach to treating IPF.
University of Delaware Professor April Kloxin wins NIH Director's New Innovator Award to develop synthetic models of idiopathic pulmonary fibrosis, a fatal disease affecting over 3 million people globally. Her research aims to uncover insights into the underlying causes and potential treatments for lung fibrosis.
A laboratory study found that fibrosis, a natural stiffening of the ovaries, occurs with age and may be linked to ovarian cancer. Metformin, a diabetes drug, was shown to halt this process in some cases.
Researchers at Temple University Health System have identified a novel signaling pathway that regulates fibrosis, a condition characterized by the formation of excessive scar tissue. By targeting this pathway, they hope to develop new treatments for fibrotic diseases, which can lead to serious health complications.
A recent study published in the New England Journal of Medicine found that nintedanib slows the progression of a broad range of scarring lung diseases. The medication was shown to be effective in patients with progressive fibrosing interstitial lung disease, regardless of the underlying cause or pattern of lung fibrosis.
Researchers found that blocking interleukin-11 protein with therapeutic antibodies can reverse lung fibrosis in a mouse model. This discovery holds promise for treating idiopathic pulmonary fibrosis (IPF), a life-threatening lung disease. Clinical trials are expected to begin by 2021.
A research team at the University of Colorado School of Medicine has identified BRD4 as a central regulator of cardiac fibroblast activation. Chemical inhibitors of BRD4 potently block cardiac fibroblast activation, providing a potential therapeutic target for heart failure treatment.
Researchers at Monash University have discovered that receptors can communicate and interact, affecting the therapeutic actions of relaxin. This finding has implications for clinical trials involving relaxin and other drugs acting on these receptors.