New study identifies targets to lessen the effects of alcoholic liver disease
A new study found that microRNA-34a contributes to liver fibrosis in ALD. Inhibiting this miR-34a reduces liver injury and fibrosis in ALD patients.
Articles tagged with Fibrosis
A new study found that microRNA-34a contributes to liver fibrosis in ALD. Inhibiting this miR-34a reduces liver injury and fibrosis in ALD patients.
Researchers have identified a new gene linked to idiopathic pulmonary fibrosis (IPF), a debilitating lung disease. The discovery suggests targeting a specific biological pathway may lead to new treatments for IPF.
Researchers at Cincinnati Children's Hospital Medical Center found that blocking a molecular pathway can stop or slow cardiac fibrosis, organ enlargement, and preserve heart function. The study provides new insights into what causes cardiac fibrosis and opens the potential for finding new therapeutic approaches.
A team of researchers from MIPT and Ghent University has created a highly realistic model that can reproduce the complexity of the cardiac microstructure, enabling scientists to better understand the causes of fibrosis and its link to arrhythmia. The model's accuracy is due in part to its consideration of cell shapes and interactions.
Researchers have discovered a class of compounds that selectively inhibit fibrosis-initiating TGF-β pathways in fibroblasts, without affecting non-fibrogenic cells. These trihydroxyphenolic compounds may provide an opportunity to treat fibrosis with fewer side effects.
A breakthrough discovery in cardiovascular fibrosis research has led to a potential treatment for multiple fibrotic human diseases. The study identified a specific cytokine as a key driver of cardiac fibrosis, paving the way for the development of first-in-class therapeutics.
Researchers at Cincinnati Children's Hospital Medical Center report encouraging preclinical results on an experimental molecular treatment for heart failure. By inhibiting a protein that regulates the heart's response to adrenaline, they alleviated disease processes in mouse models of human heart failure.
Researchers at Baylor College of Medicine found that Gata4 can reduce post-heart attack fibrosis, leading to improved cardiac function in small animal models. The study's results suggest a novel role for Gata4 in heart regeneration and may lead to new treatments for heart failure.
Researchers at Sanford Burnham Prebys and Mayo Clinic have been awarded a three-year NIH grant to identify molecules that could become new medicines to inhibit myocardial fibrosis, a major cause of heart failure. The collaboration aims to accelerate the development of novel approaches to fight disease.
Researchers at Osaka University developed a non-invasive imaging technique to detect kidney damage and predict chronic kidney disease in diabetic patients. The method uses diffusion tensor MRI (DTI) to identify specific regions of the kidney with abnormal fluid dynamics, offering a promising approach to prevent kidney disease progression.
Researchers from Helmholtz Munich found that cellular senescence in lung epithelial cells can contribute to the development and worsening of IPF. Senescent cells secrete mediators that promote fibrosis and impair lung function by preventing cell division.
Researchers develop a potential stem cell treatment for idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and cystic fibrosis by harvesting lung stem cells noninvasively and multiplying them in the lab. The therapy has shown promising results in treating IPF in rodent models.
A new sub-population of immune cells plays a key role in the development of pulmonary fibrosis. Targeting these cells could lead to new treatments with fewer adverse effects.
The Keck School of Medicine of USC has received a seven-year, $6.9 million grant from the National Institutes of Health's NHLBI to study lung cell regeneration. The research aims to develop new therapies for common lung diseases such as pulmonary fibrosis and chronic obstructive pulmonary disease.
Family members of individuals with non-alcoholic fatty liver disease (NAFLD) and cirrhosis are at a significantly higher risk of developing advanced liver fibrosis. A clinical trial found that immediate relatives had 12 times higher prevalence of liver fibrosis than healthy controls, indicating the need for screenings in family members.
CHOP researchers report universal liver fibrosis in survivors of the Fontan operation, a serious complication of the surgery. The study highlights the need for improved medical surveillance and less invasive methods to measure liver fibrosis.
Researchers have identified a protein causing liver fibrosis, paving the way for new treatments. The discovery, led by Professor Jacob George and Doctor Mohammed Eslam, reveals that variations in the interferon lambda 3 (INLF3) protein are responsible for tissue damage in the liver.
Researchers identified a key protein, SMAD3, that facilitates pro-fibrotic TGF-beta signaling. By blocking this protein, they created a peptide-carrying SNX9 that prevents SMAD3 from entering the nucleus and impacting genes regulated by TGF-beta. This approach may lead to effective treatments for fibrosis-related diseases.
Researchers found that patients with high ICOS expression had improved survival, while those with low CD28 expression had poor outcomes. The study suggests that these biomarkers may help clinicians identify IPF patients at greatest risk and develop early intervention strategies.
Recent reimbursement data shows significant variability in access to direct-acting antiviral therapy across European countries, particularly for patients with severe liver fibrosis or substance use. Many countries have restrictions on prescribing by specialists, limiting access to life-saving treatment.
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.
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.
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 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.