Articles tagged with Fibrosis
Liver fibrosis development is driven by various factors, including metabolic syndrome and insulin resistance. CD8+ T cells play a significant role in activating hepatic stellate cells, which produce scar tissue.
Researchers found that human senescent fibroblasts trigger progressive lung fibrosis in immunodeficient mice by inducing paracrine senescence and pro-fibrotic activities. The study also suggests that senolytic compounds like navitoclax can ameliorate lung fibrosis induced by senescent human fibroblasts.
A study published in Hepatology reveals that abnormal pre-mRNA splicing is associated with liver disease caused by excessive alcohol consumption. The researchers propose targeting specific splicing factors as a novel approach to mitigate the disease.
Extracellular vesicles from fibrotic lungs can activate dormant fibroblasts in healthy lungs, initiating fibrosis development and spreading. The study's findings support the potential use of EVs as a targeted drug therapy platform to slow fibrosis progression and improve patient outcomes.
Researchers have identified a potential new drug that improves both liver fibrosis and inflammation in patients with nonalcoholic steatohepatitis (NASH). The drug, Pegozafermin, mimics the body's natural hormone FGF21, controlling energy use and lipid metabolism in the liver.
A novel imaging agent has been developed to non-invasively detect pulmonary fibrosis in its early stages. The agent targets extracellular matrix fibers and has shown significant uptake in lungs with pulmonary fibrosis, matching histological results. This breakthrough could lead to earlier detection and better monitoring of the disease.
Researchers developed a more accurate model of human cardiac fibrotic tissue, which could enable quicker drug testing and potentially lead to new therapies for heart failure. The model, built using an electrospinning technique, recreates the unique aspects of scarred cardiac tissue.
Researchers found a link between short telomeres in ATII cells and lung fibrosis in post-COVID-19 patients. The study revealed loss of ATII cellularity and shorter telomeres concomitant with increased fibrotic lung parenchyma remodeling.
Research identifies Indian Hedgehog protein as a key driver of chronic kidney disease and heart damage, offering new hope for treatments. The findings suggest that blocking the protein's actions could improve kidney function and reduce cardiovascular risk.
Researchers found variant cells in lungs of IPF patients that can drive fibrosis and inflammation. These cells may be targeted for future therapy, offering new hope for treatment.
Researchers discover that senescence-associated secretory phenotype (SASP) can induce neuroendocrine transdifferentiation (NED) in breast cancer epithelial cells, promoting tumor progression and aging-related features. SASP's dual role in cancer involves both antitumoral and tumorigenic effects.
Vogel and Benn's study replicates tissue growth in vitro, revealing the importance of ECM interactions. Myofibroblasts play a key role in wound healing and cancer progression, but their transformation into fibroblasts is influenced by ECM composition and structure.
Researchers discovered ERK signalling is a crucial switch between scarring and regeneration, with prolonged activation promoting regenerative success. Modulating ERK activity could potentially stimulate regeneration in clinical settings.
This study examined the effects of deferoxamine and ferrostatin-1 on salivary gland dysfunction in ovariectomized rats. The researchers found that these compounds reduced inflammation, fibrosis, and improved salivary gland function, suggesting potential treatments for postmenopausal xerostomia.
A new study published in The Lancet shows that metabolic surgery is more effective than medications and lifestyle interventions in treating advanced non-alcoholic fatty liver disease. The trial compared three active treatments and found that surgery reversed inflammation and improved liver fibrosis, leading to better overall health ben...
Researchers have discovered that manipulating Yes-associated protein (YAP) expression in liver progenitor cells can improve their ability to regenerate and repair liver tissue. This could lead to new treatments for chronic liver diseases.
The American Roentgen Ray Society presents its 2023 Honorary Lecture on Advanced High-Resolution CT, dedicated to the late Dr. W. Richard Webb, who transformed thoracic imaging with his foundational work in HRCT. The lecture explores multiple conditions diagnosed via HRCT and the radiologist's role on multidisciplinary teams.
Small vesicles released by intestinal bacteria induce immune activation and progression of liver cirrhosis, as well as reduction of serum albumin level, leading to edema and ascites in patients with cirrhosis.
A study by University of Rochester Medical Center researchers reveals how a biological clock molecule contributes to lung scarring. Low levels of REV-ERBα have been linked to increased collagen production and worse lung damage in patients with pulmonary fibrosis.
Human macrophages use Siglec-14 receptors to recognize and engulf carbon nanotubes, leading to inflammation. The discovery could pave the way for developing safer carbon nanotubes and therapies to prevent inflammatory diseases.
Researchers at TUM have developed a method to create mini-hearts in Petri dishes using stem cells. The resulting organoids mimic the earliest stages of human heart development and can be used to investigate congenital heart defects, potentially leading to new treatment methods.
Scientists have identified an autoinflammatory disease called Lyn kinase-associated vasculopathy and liver fibrosis (LAVLI) linked to mutations in the LYN gene. The research suggests that Lyn kinase may be a potential therapeutic target for drugs treating non-syndromic small vessel vasculitis and inflammation-induced liver fibrosis.
Researchers from Kyushu University found that the single mechanosensitive protein VGLL3 induces fibrosis, thickening and scarring tissue. The study suggests targeting this protein could lead to new treatments against fibrosis.
A study published in Cell Death & Disease reveals that a protein cross-linking enzyme called TG2 exacerbates kidney fibrosis by polarizing M2 macrophages. The researchers hope to develop treatments for diseases caused by inflammation imbalance, such as fibrosis, cancer, and atherosclerosis.
Researchers found that senescence-associated exosomes (SA-EXOs) from MSCs induce fibrosis and activate invasive characteristics in neighboring cells via the TGF-β pathway. SA-EXOs play a large role in cancer-related fibrosis, and their unique miRNA content influences myofibroblast phenotypes.
Researchers discovered that lipid deposition on medical implant surfaces can signal to the immune system whether to attack or ignore the implant. This knowledge could help develop biomaterials that deflect host immune aggression, reducing malfunction rates for devices like pacemakers and surgical mesh.
A new study found that Black patients with pulmonary fibrosis are significantly younger than their Hispanic and white counterparts, experiencing accelerated disease progression. Lifestyle and socioeconomic factors linked to environmental exposures may contribute to these disparities.
Researchers at Mass General Hospital have found that intestinal fibrosis plays a critical role in the progression of inflammatory bowel disease (IBD), affecting the growth and differentiation of intestinal stem cells. The study suggests targeting mechanosensing pathways may offer an attractive therapeutic strategy for IBD.
A study published in Radiology revealed persistent lung abnormalities in patients two years after COVID-19, including fibrosis and cystic changes. The incidence of lung abnormalities gradually decreased over time, but the proportion of fibrotic interstitial lung abnormalities remained stable.
Researchers identified a protein in lung cells that blocks SARS-CoV-2 infection and forms a natural protective barrier. The discovery opens up an entirely new area of immunology research around LRRC15 and offers promising prospects for developing new drugs to prevent viral infection or treat fibrosis in the lungs.
A mutant SRSF1 gene may cause severe nonalcoholic fatty liver disease (NASH), researchers have found. Mice lacking the gene develop all three hallmarks of NASH: excess fat, inflammation, and scarring in the liver. The study suggests that DNA damage in liver cells triggers this pathology, highlighting the need to protect the genome.
Scientists at Duke-NUS Medical School and NHCS have discovered that blocking an immune-regulating protein called interleukin-11 enables damaged kidney cells to regenerate, restoring impaired kidney function. This breakthrough suggests a new approach for treating chronic kidney disease.
A study published in JACC: Clinical Electrophysiology found a significant correlation between periodontitis and fibrosis in the left atrium, which can lead to atrial fibrillation. Researchers suggest that periodontal care could aid in comprehensive management of atrial fibrillation.
Researchers at Aston University are working with Isterian Biotech to develop small molecule inhibitors targeting transglutaminase 2, a key enzyme in fibrosis. The goal is to stop or reverse pathological crosslinking of proteins that lead to fibrotic diseases such as idiopathic pulmonary fibrosis.
Researchers found that regorafenib, a dual PDGFR α/β inhibitor, modifies the cancer microenvironment and enhances the efficacy of anti-PD-1 immunotherapy in advanced gastric cancers. This combination therapy boosts tumor infiltrating immune cells and reduces tumor fibroblasts.
A new study by the University of Coimbra found that higher coffee intake is associated with reduced NAFLD severity in overweight people with T2D. Caffeine and polyphenols in coffee may help alleviate liver fibrosis and improve glucose homeostasis.
Researchers at the University of Colorado School of Medicine have discovered a new mechanism for slowing scarring of heart tissue, a process known as cardiac fibrosis. The study's findings suggest that inhibiting the degradation of eicosanoids may be a promising approach to preventing or reversing cardiac fibrosis.
Researchers found that MMTV-NeuT/ATTAC mice treated with anti-PD-1 therapy developed increased tumor-associated macrophages, EMT, fibroblast proliferation, and enhanced extracellular matrix. These findings suggest potential therapeutic avenues to enhance PD-1 immune checkpoint sensitivity.
Macrophage PPARγ acetylation decreases energy expenditure and worsens insulin sensitivity, glucose tolerance, and lipid metabolism in mice fed a high-fat diet. This impairment promotes macrophage infiltration, adipose fibrosis, and hepatic steatosis.
Researchers found that P2-HNF4α expression is associated with p-STAT3 and c-Myc expression in NAFLD patients, suggesting potential biomarkers for hepatocellular carcinoma (HCC) risk. Additionally, p-STAT3 expression was linked to hypertension, while c-Myc expression was associated with advanced fibrosis.
A new study found that up to 11% of hospitalized COVID patients have fibrotic patterning in their lungs after recovery, which can lead to breathing difficulties and decreased life expectancy. The study suggests that these patients require close follow-up care, including repeat radiological imaging and lung function testing.
A new study finds that COVID-19 patients exhibit higher liver stiffness months after infection, indicating possible long-term liver damage. The study also suggests that even pre-pandemic patients showed increased liver stiffness, likely due to changing referral patterns during the pandemic.
A study by UTHealth Houston reveals a unique fibrotic gene signature in non-resolvable COVID-19 patients, who experience prolonged pulmonary effects following infection. Lung transplantation is often required for survival due to the rapid progression of damage to lung tissue.
A new study using photon-counting CT technology has shown that it can detect more post-COVID-19 lung damage than conventional CT scans, particularly in patients with persistent symptoms. The technology may lead to earlier treatment and better outcomes for those affected by COVID-related lung damage.
Researchers developed a nanofiber aerogel that promotes faster and more effective healing of diabetic wounds. The aerogel facilitates cell migration, oxygen, and nutrient delivery to the wound bed, while incorporating an anti-microbial peptide prevents bacterial growth and promotes healing.
Researchers at UCalgary have discovered a potential new treatment for fibrosis, a condition that causes thickening of the gut wall and life-threatening blockage in people with Crohn's disease and ulcerative colitis. The study suggests that drugs targeting specific sensors may prevent inflammation-associated gut blockage.
Researchers found that first-degree relatives of patients with advanced fibrosis are at a 15% risk of developing nonalcoholic fatty liver disease. Early screening for advanced fibrosis among siblings and offspring of patients can help prevent the progression to cirrhosis or liver failure.
Researchers at CNIO have identified alveolar type II pneumocytes as the primary cell type responsible for developing pulmonary fibrosis. The study reveals that targeting these cells through telomere-based therapy may lead to a breakthrough in treating this debilitating disease.
A new automated screening tool can accurately identify patients at high risk of developing progressive scarring of the lungs, a condition called idiopathic pulmonary fibrosis (IPF). The tool uses machine-learning algorithms to analyze patient electronic health records and detects IPF risk automatically.
Researchers at Medical University of South Carolina found that scleroderma patients have reduced levels of antifibrotic protein Cathepsin L, packaged in an inactive state. Increasing Cathepsin L levels and function could have therapeutic benefits for patients with lung fibrosis.
Researchers developed a universal screening tool for IPF that can alert primary care physicians to its possible presence, enabling earlier diagnosis and treatment. The Zero-burden Co-Morbidity Risk Score for IPF (ZCoR-IPF) algorithm uses existing patient records to identify patients at risk of developing the disease.
A study identifies a molecule called NIK that promotes the growth of bile duct cells in the liver, leading to scarring and liver fibrosis. Removing NIK or blocking its action with inhibitors may prevent disease progression.
A new Chinese Medical Journal review article elucidates the potential contributors to non-alcoholic fatty liver disease (NAFLD) progression, highlighting the role of bile acid and sphingolipid biology. Researchers summarize current understanding of NAFLD, its progression, and potential therapeutic strategies.
The September issue of CHEST journal features 40 articles on clinically relevant topics, including disparities in rural populations with idiopathic pulmonary fibrosis. The journal also offers complementary web and multimedia activities to expand its reach.
Researchers at the University of Zurich have developed a new immunotherapy strategy to eliminate fibroblasts in targeted manner, reducing lung and liver fibrosis in mice. The treatment triggers an immune response via cytotoxic T-cells, eliminating activated connective tissue cells while leaving resting cells undamaged.
A substance produced by gut microorganisms, TMAO, can lead to scarring and vascular damage in scleroderma. The Western diet rich in meat contributes to TMAO formation, which reprograms cells to become scar-forming myofibroblasts.
Researchers have discovered a molecule that can suppress the development of kidney fibrosis, a condition leading to kidney failure and devastating consequences. The breakthrough could lead to the development of new drug treatments for millions of people affected by chronic kidney disease.
The study investigated the effects of combined endocrine-disrupting chemicals (EDCs) on liver function and metabolic homeostasis in mice models. Significant changes were observed at high EDC exposure levels, including liver weight increase, lipid buildup, and elevated blood glucose levels.
A Nagoya University research group has developed an AI algorithm that can diagnose idiopathic pulmonary fibrosis with high accuracy, based on non-invasive examinations and medical data. The technology may revolutionize medical care by allowing doctors to request AI-assisted diagnoses instead of specialists.
Researchers identified common cellular mechanisms and dysfunctional processes driving post-COVID lung disease, similar to idiopathic pulmonary fibrosis. The study found shared gene expression patterns and endoplasmic reticulum stress as early triggers of both conditions.