Articles tagged with Fibrosis
A new study published in JCI Insights reveals that increasing SMOC2 levels in the kidney can initiate and continue kidney fibrosis, while reducing SMOC2 levels prevents it. Detecting SMOC2 in urine may help diagnose fibrosis, making it a potential biomarker for early intervention.
Researchers at Stanford University School of Medicine identified a pathway that drives fibrosis in many organs, including scleroderma and idiopathic pulmonary fibrosis. Blocking the CD-47 signal reverses lung fibrosis in mice.
A new collagen-targeting PET probe, Ga-CBP8, has shown promise in diagnosing and staging pulmonary fibrosis, as well as monitoring treatment response. The probe can differentiate between stable disease and progressive fibrosis, allowing for more effective treatment planning.
Researchers have developed an effective antibody against radiation-induced pulmonary fibrosis, a debilitating side effect of lung cancer treatment. The antibody targets connective tissue growth factor (CTGF), reversing fibrotic transformation and improving pulmonary function in mice.
Researchers at MIT and Boston Children's Hospital have identified a key signaling molecule that triggers the formation of scar tissue around implantable medical devices. Blocking this molecule prevents scar tissue from forming, extending the lifespan of devices such as glucose sensors, pacemakers, and insulin delivery systems.
Researchers found that markers of cellular senescence were higher in individuals with idiopathic pulmonary fibrosis, and senescent cell burden increased with the progression of the disease. The findings suggest targeting senescent cells could be a viable treatment option for individuals suffering from idiopathic pulmonary fibrosis.
Researchers at the Medical University of South Carolina discover a peptide that reverses cardiac fibrosis and improves heart function without toxicity. The study uses a transverse aortic constriction mouse model to demonstrate the peptide's effectiveness in halting and reversing fibrotic ventricular wall thickness.
Researchers at Boston Children's Hospital have identified a potential therapeutic solution for age-related fibrosis by pinpointing the gene responsible for the condition. Deletion of the PAD4 gene has been shown to curb fibrosis in mice, reducing organ dysfunction and improving heart function.
A recent international multicenter study has identified a molecule that can help personalize treatment for heart failure. Researchers have found that an excess of lysyl oxidase-like 2 produces fibrosis of the cardiac muscle, impeding its normal functioning and stimulating HF development. The elimination of this excess repairs fibrosis ...
Researchers at Osaka University discovered a new subgroup of monocytes called SatM, which may contribute to fibrosis. These cells showed characteristics that suggested they were hybrids of different immune cells and can be regulated by C/EBPβ.
Researchers found a link between the loss of hyaluronan and AEC2 stem cell failure, leading to scarring in lungs. The study highlights potential treatment pathways using drugs that stimulate AEC2 cell reproduction.
Researchers found that fat-free mass index, but not body mass index, was a significant predictor of survival in patients with idiopathic pulmonary fibrosis. Lower fat-free mass index was linked to worse survival over an average follow-up of 2.3 years.
Researchers at Hospital for Special Surgery have identified a population of stem cells called ADSCs that are reduced in number in the layer of fat sitting under the skin in patients with scleroderma. The study found that replenishing these cells with antibodies may reverse the fibrosis characteristic of the disease.
Researchers at Columbia University Medical Center discovered that inactivating the TAZ protein in liver cells reverses fibrosis, a primary feature of nonalcoholic fatty liver disease. This finding has potential implications for treating nonalcoholic steatohepatitis, a serious condition that can lead to liver failure and cancer.
A Japanese research team has identified a hormone that limits liver fibrosis in nonalcoholic steatohepatitis (NASH) and cirrhosis. Administering growth hormone alleviated NASH conditions caused by adult growth hormone deficiency, and treatments were effective on model animals.
Researchers developed a novel method to quantify NAFLD progression to advanced fibrosis and cirrhosis. The technique combines multiple non-invasive measures, including heavy water labeling and MRI assessments, to predict individual clinical fibrotic disease progression.
Scientists at the University of British Columbia have made a groundbreaking discovery that could lead to treatments for fibrosis in Crohn's patients. Researchers found a mutation in mice that prevented fibrosis after infection, targeting a hormone receptor responsible for stimulating part of the immune response.
Researchers aim to understand the genetics and underlying biological mechanisms that lead to IPF. They will analyze genetic information on over 1,200 families to identify new genes causing the disease.
Researchers identified a new gene, NAF1, associated with pulmonary fibrosis-emphysema in people with abnormally short telomeres. The mutation affects telomerase RNA stability, leading to decreased telomerase levels and increased risk of lung disease.
A study published by Cincinnati Children's Hospital Medical Center reveals the molecular pathways responsible for heart anomalies in sickle cell anemia. The research opens a path to non-invasive diagnosis and development of new targeted therapies, aiming to improve quality of life and reduce mortality among SCA patients.
Researchers link vitamin A metabolism to eye fibrosis, finding that retinoic acid triggers fibroblast signaling promoting scarring. Inhibiting aldehyde dehydrogenase may prevent ocular fibrosis.
Researchers utilized Regeneration Intelligence to evaluate signaling pathways in lung and liver fibrosis and glaucoma, identifying potential biomarkers and therapeutic targets. The study suggests that pathway signatures may play a role in aging-related diseases.
A Canadian study discovered that a specific kind of bile acid can prevent cardiac fibrosis, a condition leading to heart failure. Researchers are now exploring the therapeutic effect in humans and aiming to understand the molecular mechanisms behind this breakthrough.
A new study published at EULAR 2016 found that oestrogens significantly slow down fibrosis in experimental models representative of systemic sclerosis. This could lead to the development of potential hormone therapies for this difficult-to-treat condition.
The review assesses the fibrotic potential of various nanomaterials, including multi-walled carbon nanotubes, and recommends in vitro approaches to predict lung fibrosis development. This scientific study aims to advance non-animal methods for studying nanomaterial effects on human health.
Researchers found that myocardial fibrosis in obstructive sleep apnea patients is associated with increased risk of heart failure hospitalization and death. The study suggests that quantifying myocardial fibrosis could help identify patients at higher risk, paving the way for a personalized approach to treating cardiovascular disease.
A new imaging method reveals that IPF foci are complex structures with diverse shapes and sizes, forming at discrete sites of lung injury. This breakthrough may help researchers comprehend the relationship between fibroblastic foci and disease progression in IPF patients.
Researchers at the Medical University of South Carolina discovered that the M10 peptide protects against fibrotic damage in a mouse model of ILD and is likely due to its modulation of the TGF-β1 pathway. The anti-fibrotic effects of M10 may also be effective in treating other forms of pulmonary fibrosis.
A vaccine developed for smallpox improved lung function in a mouse model of idiopathic pulmonary fibrosis by inducing resident memory CD4+ T cells. This immune response was associated with reduced fibrosis and increased survival rates.
Researchers developed a novel 3D imaging technique that provides accurate detection of advanced fibrosis in liver disease. The technology outperforms current methods, offering improved accuracy and reduced invasiveness.
A study led by Dr. Roger J. Hajjar and Dr. Woo Jin Park found that CCN5 protein can reverse established cardiac fibrosis in heart failure models. The researchers used trichrome staining to show the reversal of cardiac fibrosis, demonstrating potential for new anti-cardiac fibrosis therapies.
Researchers found that inhibiting Wnt secretion can prevent the build-up of scar tissue in kidneys and protect against renal fibrosis. This suggests a novel therapeutic approach to treating kidney disease.
Researchers found a compound that prevents scarring in the lungs and liver also shows promise in preventing pancreatic fibrosis. The study used an animal model to demonstrate the effectiveness of the integrin inhibitor in halting fibrosis and potentially preserving pancreatic function.
Researchers have found a modified protein that can reverse liver fibrosis and cirrhosis in lab rats. The protein, TRAIL, was coated with a polymer to extend its half-life, allowing it to effectively kill activated hepatic stellate cells and reduce signs of fibrosis.
Researchers found nearly half of IPF-related websites recommended medications with no proven benefit, while more than a third suggested harmful treatments. The top two accurate sources were Wikipedia and Medscape.
A study in JCI Insight identifies Dickkopf-3 as a driver of renal fibrosis in chronic kidney disease. DKK3 expression is elevated in stressed tubular epithelia and associates with profibrotic T cell responses, leading to interstitial fibrosis and impaired kidney function.
Researchers found mild fibrosis in biopsies taken a few months after transplant correlated with acute kidney injury gene expression, while advanced fibrosis reflected ongoing injury. Older transplants with fibrosis were associated with an increased risk of kidney failure.
Researchers at NYU Langone developed an antiscarring paste that inhibits fibrosis caused by radiation therapy in mice. The study suggests the use of A2A receptor blockers as a potential therapeutic approach to prevent scarring and fibrosis in cancer patients.
The Salk Institute has identified a drug called JQ1 that prevents and reverses liver fibrosis in animals, a condition that replaces normal liver cells with scar tissue until the organ no longer works. This discovery may also treat fibrosis in other organs such as the lung, pancreas, and kidney.
Researchers have discovered a new molecule involved in the development of fibrosis, a condition characterized by inflammation and stiffening of skin tissue. High levels of this molecule, fibulin-5, were found to contribute to increased skin tissue inflammation and stiffening.
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.
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.
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.
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.