Articles tagged with Fibrosis
Researchers found that fatty liver disease and scarring have a significant genetic component, with heritability rates of around 50%. The study used twin analysis to show that monozygotic twins were more likely to share similar levels of fat content and liver stiffness.
Researchers have identified a naturally occurring blood protein called lumican as a key player in the development of excessive scar tissue in fibrotic diseases. The study suggests that lumican triggers a vicious cycle when stimulated by tumor necrosis factor alpha, leading to increased production of scar tissue.
Exposure to high-concentration airborne particulate matter PM2.5 has been shown to directly affect the liver, triggering liver fibrosis in animal models. The study highlights air pollution as an independent risk factor for liver fibrosis, with implications for medical care and health policy-making.
A new study reveals liver fibrosis affects 5.6% of adults aged ?45, primarily those with diabetes or steatosis. The rising prevalence highlights the growing concern of liver health issues due to an aging population and increasing rates of diabetes and obesity.
Scientists at University of Texas MD Anderson Cancer Center identified EMT as a potential therapeutic target for reversing kidney disease and fibrosis. The study showed that inhibiting EMT in tubular epithelial cells can restore their health and function.
Researchers have demonstrated a direct connection between two signaling proteins (NOX1 and NOX4) and liver fibrosis, a scarring process underlying chronic liver disease. The study adds credence to a pharmaceutical effort to create new treatments for diabetic nephropathy, liver fibrosis, and other progressive fibrotic diseases.
Proteins in the Wnt signaling pathway play a critical role in driving kidney scarring, which can lead to chronic kidney disease. Boosting expression of Wnt proteins in healthy kidneys may be an effective strategy for treating chronic kidney disease.
A novel mass spectrometry technique has enabled scientists to quantify and profile dynamic changes in lung tissue composition during regeneration. The study reveals the importance of extracellular matrix proteins in activating stem cells, offering a new avenue for treating chronic lung diseases like pulmonary fibrosis.
CNIO researchers discover that telomeres are at the origin of idiopathic pulmonary fibrosis, a disease with no current treatment. The study reveals that telomere damage triggers progressive pulmonary fibrosis in mice, suggesting new therapeutic strategies based on telomerase activation.
Researchers at Brown University have discovered a molecular mechanism behind pulmonary fibrosis in Hermansky-Pudlak syndrome patients. They propose two therapeutic strategies: manipulating CHI3L1 and CRTH2 proteins to slow down scarring.
Researchers found significant decreases in skin scarring and expression of molecular markers after treating SSc patients with fresolimumab. The study suggests that targeting TGF-beta may provide a major treatment advance for scarring-mediated organ dysfunction.
A recent study published in Respirology found that patients with idiopathic pulmonary fibrosis (IPF) have significantly shorter telomere lengths than healthy individuals. The study suggests that mutations in the enzyme responsible for maintaining full-length telomeres may play a key role in the development of IPF.
Researchers at UGA have discovered a potential treatment for pulmonary fibrosis and pulmonary hypertension using the drug triciribine. The study shows that triciribine can halt disease progression and may even reverse some of the damage to lung tissue.
Researchers identified mutations in PARN and RTEL1 genes, which cause excessive telomere shortening and lung scarring disease. The findings strengthen the link between lung fibrosis and telomere dysfunction.
A study reveals that individuals with undiagnosed hepatitis C infection have a similar risk of developing advanced liver fibrosis as those who are diagnosed. The findings support the importance of regular screening for HCV, especially in high-risk groups.
Capsaicin, the active compound in chili peppers, has been found to have beneficial effects on liver damage. In a study, capsaicin reduced the activation of hepatic stellate cells, which are involved in liver fibrosis. The compound partially improved liver damage and inhibited further progression of the injury in mice models.
A new study presented at The International Liver Congress 2015 shows that significant weight loss through lifestyle changes can improve histological features of non-alcoholic steatohepatitis (NASH). Over 10% weight loss is necessary to induce complete resolution of steatohepatitis, fibrosis, and portal inflammation.
Researchers have identified a promising new target for treating pulmonary fibrosis, a severe and chronic lung disease. By inhibiting the enzyme prolyl 4-hydroxylase, which promotes collagen production, researchers aim to reduce excessive fibrous tissue growth.
A new molecule, endosialin, on hepatic stellate cells drives liver fibrosis by activating these cells. However, its absence improved the regenerative capacity of remaining liver cells without proliferating them. This finding helps understand how liver fibrosis develops and may lead to treatments for other diseases.
Researchers found that cathelicidin protein can prevent intestinal fibrosis and scarring in colitis, potentially sparing patients from repeated surgeries. The study used pre-clinical models of disease and human colonic fibroblasts to demonstrate the anti-fibrotic effects of cathelicidin.
A study at MD Anderson Cancer Center found PRM-151 to be well-tolerated in patients with advanced myelofibrosis, showing encouraging trends in clinical and histologic aspects of the disease. The therapy demonstrated reduced bone marrow fibrosis and improved hematologic parameters, suggesting potential for further development.
Fibrotic diseases cause up to 45 percent of deaths worldwide. Researchers identified Gli1 cells around blood vessels as responsible for fibrosis. Abating these cells improved organ function in mice with kidney and cardiac fibrosis.
A Penn study found that a defect in energy production plays a key role in CKD development. Restoring fatty acid metabolism largely prevented signs of CKD in mouse models. The researchers hope to develop new compounds that boost enzymes related to fatty acid metabolism to slow CKD progression.
A genetic marker in the SHROOM3 gene has been found to be associated with increased fibrosis and function loss in kidney transplants. Researchers hope this discovery will lead to improved screening of potential donors and development of new drugs to prevent disease progression.
Researchers at Harvard University have identified a rare population of stem cells that give rise to fibrosis, a condition characterized by the buildup of scar tissue in organs. The study suggests that targeting these stem cells could lead to therapeutic breakthroughs for conditions such as diabetes, lung disease, and high blood pressure.
A study found that excess fat around the heart, measured by epicardial adipose tissue volume, is more closely associated with atrial fibrillation than BMI. The layer of fat was shown to correlate with scarring in the left atrium, increasing the risk of irregular heartbeat.
A study found that patients with chronic hepatitis C virus infection and advanced fibrosis or cirrhosis who attain SVR have survival rates comparable to those of the general population. However, patients without SVR experience reduced overall survival.
A study found that excessive myofibroblast activity during wound healing leads to increased ECM organization, promoting the release of active TGF-β1. This activation then induces further myofibroblast activity and fibrosis.
Researchers at Yale University have discovered a microRNA mimic, miR-29, that can reverse the effects of pulmonary fibrosis in mouse models. The treatment uses intravenous delivery and has shown sustained effects on lung tissue. Further studies are needed to evaluate its therapeutic potential for human idiopathic pulmonary fibrosis.
Researchers found that transplanting B10 human bone marrow-derived mesenchymal stem cells into the bladder wall of mice with spinal cord injury improved bladder function by promoting the growth of smooth muscle cells. This study provides potential evidence for MSC-based cell transplantation as a novel therapeutic strategy for bladder d...
A study has identified chitinase 3-like-1 (CHI3L1) as the master regulator of idiopathic pulmonary fibrosis (IPF), a devastating lung disease. CHI3L1 plays a dual role in promoting tissue repair and reducing cell death, but its chronic elevation contributes to excessive scarring and tissue dysfunction.
Two drugs, pirfenidone and nintedanib, have been found to slow the progression of idiopathic pulmonary fibrosis, a fatal lung disease. Researchers conducted multicenter clinical trials to test their efficacy.
Researchers at the University of Illinois Chicago have discovered a protein molecule that slows the progression of pulmonary fibrosis, a deadly lung disease. The protein, LYCAT, is found to be protective and may boost survival rates in patients with idiopathic pulmonary fibrosis.
Bariatric surgery resolves liver inflammation and reverses early-stage liver fibrosis by reducing fat deposits in the liver. The procedure showed significant improvement in nonalcoholic fatty liver disease (NAFLD) in severely obese patients.
A new study reveals that even light drinking increases the risk of liver fibrosis in people co-infected with HIV and hepatitis C virus (HCV) infection. Researchers found a stark difference between co-infected and uninfected groups, highlighting the importance of counseling patients to reduce alcohol consumption.
A Northwestern University discovery identifies a specific protein, fibronectin (FnEDA), as a key player in promoting fibrosis in people with scleroderma. The study found that blocking this protein's activity can prevent skin fibrosis in mice, offering new avenues for treatment.
Researchers at Michigan State University have identified the core signaling pathway that activates scleroderma and found chemical compounds that can turn it off. This discovery offers a new approach to treating the disease, which currently lacks effective treatments.
Scientists at the University of Sheffield have developed a novel antibody-based therapy to target fibrosis progression. The treatment blocks key enzyme action and may also work for lung, liver, and heart fibrosis.
A Cedars-Sinai research team led by Paul W. Noble is developing a novel approach to treat idiopathic pulmonary fibrosis, a disease that destroys the lungs and damages vital organs. The two-year study aims to build upon preliminary research and uncover the precise way normal lung stem cell repair occurs.
Scientists at Saint Louis University have discovered a potential novel therapeutic approach to treat fibrotic diseases by targeting the Transforming Growth Factor (TGF) beta protein. Removing a gene that makes alpha v integrins blocks TGF beta activation, and treatment with a small molecule compound replicates this effect.
Research published in Hepatology suggests that estrogen has a protective effect against the development of severe liver fibrosis in patients with nonalcoholic steatohepatitis (NASH). The study found that men and post-menopausal women have similar risks of developing severe fibrosis compared to pre-menopausal women.
Researchers found ionizing radiation exposure promotes formation of fusion oncogenes in papillary thyroid cancers. In another study, the origin of lethal prostate cancer was traced back to a small, low-grade focus in the primary tumor. Additionally, reduced reactive oxygen species production in diabetic kidneys may contribute to diseas...
Researchers at the University of Tsukuba have identified a synthetic ligand that reduces renal fibrosis in mice by inhibiting the TGF-β/SMAD signaling pathway. This finding has implications for the treatment of patients with fibrotic diseases.
Researchers at Johns Hopkins Medicine have identified a defect in cell communication as the likely cause of systemic sclerosis, a disease affecting approximately 100,000 people in the US. They also developed treatment strategies using compounds that target the immune response and fibrosis.
A new imaging technique, MRE, can accurately detect fibrosis in children with chronic liver disease, including non-alcoholic fatty liver disease. The study showed high accuracy in detecting advanced fibrosis in obese patients, potentially reducing the need for costly and invasive liver biopsies.
Myocardial interstitial fibrosis is a major therapeutic target for the prevention and treatment of heart failure. The FIBRO-TARGETS project will accurately identify key mechanisms involved in fibrosis and define therapeutic approaches to target these mechanisms.
A new study shows that magnetic resonance imaging (MRI) can stage the degree of damaged heart tissue and help predict whether treatment will be successful. Patients with early-stage atrial fibrosis have a higher chance of being cured, while those with late-stage fibrosis have a lower success rate.
A recent study published in Immunity has identified interleukin-33 as a central factor in the formation of liver fibrosis. The research suggests that targeting this molecule could provide a promising new approach to protecting against liver fibrosis and chronic liver disease.
A study published in Spine Journal found that 65% of herniated lumbar discs resulted from avulsion of the vertebral end plate junction, rather than true rupture. The findings challenge conventional wisdom on how herniated discs occur and may lead to a reevaluation of treatment strategies.
Scientists have identified four pathways involved in the formation of myofibroblasts that drive destructive runaway scarring in organs. These pathways provide leads for drug targets to control fibrosis.
A common genetic variant of the MUC5B gene is linked to an increased risk of interstitial lung disease and symptoms such as shortness of breath and cough. The study suggests that this variant may be a key indicator for predicting individuals at risk for pulmonary fibrosis, potentially paving the way for prevention efforts.
A study published in JAMA Network found that genetic variation in the MUC5B gene is associated with improved survival rates among patients with pulmonary fibrosis. The research suggests that this genetic variant can be used to predict mortality in these patients, providing new insights into the underlying mechanisms of the disease.
Researchers found a genetic risk factor for pulmonary fibrosis in people with the MUC5B gene variant, associated with increased lung inflammation and scarring. The study suggests that pulmonary fibrosis may be part of a larger syndrome, potentially leading to early detection and treatment.
A study published in JAMA found that a specific genetic variation is associated with improved survival in some cases of pulmonary fibrosis. The researchers identified the MUC5B promoter polymorphism as a key factor, which may lead to the development of new treatments for this deadly lung disease.
Scientists at the Salk Institute have discovered that a synthetic form of vitamin D can deactivate the switch governing fibrotic response in mouse liver cells, suggesting a potential new therapy for fibrotic diseases. This finding could lead to the development of a safer and more effective treatment for liver fibrosis.
A genome-wide association study of over 6,000 people has identified seven new genetic regions linked to pulmonary fibrosis. The research provides clues to the disease's mechanisms and suggests a possible connection between genetic variants and environmental factors.
A genome-wide association study identified a novel genetic locus linked to both the onset and mortality of idiopathic pulmonary fibrosis. The study found that a variant in the TOLLIP gene was associated with an increased risk of death, suggesting an abnormal immune response may be central to the disease.
Pulmonary fibrosis is a condition where lung tissue becomes thickened and scarred, with no approved drugs for its most common form. A new study found that genetic variation accounts for approximately one-third of the risk, identifying seven novel genetic risk loci involved in host defense, cell-cell adhesion, and DNA repair.
Researchers have identified two key compounds produced by mast cells that promote fibrogenesis, leading to pulmonary fibrosis. Introducing mast cells into mice lungs can reverse disease protection and cause pulmonary fibrosis.
Patients with nonalcoholic fatty liver disease (NAFLD) without advanced fibrosis do not have higher mortality risk, according to new research. However, those likely to progress to advanced fibrosis had a 69% increase in mortality compared to those without fibrosis.