Articles tagged with Fibrosis
Researchers at the University of Trento have developed a genome editing strategy to permanently correct two types of mutations that cause cystic fibrosis. The 'SpliceFix' technique uses Crispr-Cas to edit patient-derived organoids, showing high precision and efficacy.
Michelle Long, MD, MSc, assistant professor of medicine at Boston University School of Medicine, has been awarded a three-year, $495,000 Doris Duke Clinical Scientist Development Award to investigate the relationship between physical activity and NAFLD. The study aims to identify biomarkers of early disease and risk for progression.
A recent study published in PLoS One found a link between the gene AEBP1 and severe liver damage, specifically nonalcoholic steatohepatitis. The research suggests that AEBP1 regulates a network of genes related to fibrosis, which could lead to new therapeutic targets for treating liver disease.
Lung scarring can lead to pulmonary fibrosis and life-threatening complications. Researchers found increased MMP activity in lung tissue affected by Hermansky-Pudlak syndrome, suggesting a new link for diagnosis and treatment.
Researchers at St. Jude Children's Research Hospital have discovered an association between a mutation in the NEU1 gene and fibrotic conditions, including idiopathic pulmonary fibrosis. The study found that mice lacking the Neu1 gene developed muscle atrophy due to excessive connective tissue production.
MIT researchers have created a novel way to encapsulate islet cells, which they are developing as a possible treatment for patients with type 1 diabetes. The crystallized drug formulation prevents immune system rejection and allows the device to function for more than a year.
Researchers identified several potential therapeutic targets for Alport syndrome, including bardoxolone and anti-miRNA21. The disease is characterized by progressive kidney damage and proteinuria, and current treatments are primarily aimed at slowing disease progression rather than halting it.
Researchers at Georgia State University have developed a non-invasive method for detecting liver fibrosis using machine-learning algorithms and ultrasound scans. This technology has the potential to improve early diagnosis and treatment of liver diseases, which affect millions worldwide.
A joint ATS and European Respiratory Society statement reveals that occupational hazards contribute to over 1 in 10 cases of non-cancerous lung diseases, including asthma and COPD. The study estimates the burden of these conditions, highlighting a need for policy makers to prioritize prevention among working women and men worldwide.
Researchers at Cincinnati Children's Hospital Medical Center develop human liver organoids that accurately mimic key features of fatal liver diseases. The study reveals molecular secrets of deadly ailments and tests a potential therapy for Wolman disease, reversing an often-fatal childhood condition.
A study using praliciguat to stimulate soluble guanylate cyclase found that it can inhibit inflammation and fibrosis in liver cells, suggesting a potential therapy for nonalcoholic steatohepatitis. The results also indicate that praliciguat may suppress stellate cell fibrotic transformation.
Researchers developed a capsule-shaped photoacoustic imaging endoscope to examine intestinal changes in Crohn's disease. The device can differentiate between inflammatory and fibrotic strictures, allowing for more targeted treatment and potentially reducing adverse effects. This technology could also provide real-time diagnostic inform...
Researchers have discovered a potential new treatment for renal fibrosis by selectively activating AT1 receptors on T cells, which may help limit scar formation in the kidney. The study found that activating these receptors mitigates renal fibrogenesis by inhibiting Th1 differentiation and renal accumulation of pro-fibrotic macrophages.
A study of over 4,000 young adults in the UK found that nearly 20% had nonalcoholic fatty liver disease, and one in 40 had advanced fibrosis. The condition is linked to obesity, diabetes, and hyperlipidaemia, highlighting the need for greater public health awareness.
Researchers found that serum AKR1B10 levels were significantly associated with advanced liver fibrosis stages, particularly stage 4. The protein's origin was confirmed via immunohistochemical staining, and its combination with WFA(+)-M2BP showed high sensitivity and specificity for predicting NASH fibrosis and life-threatening events.
The Phase 3 REGENERATE study confirms obeticholic acid's effectiveness in treating NASH with liver fibrosis, improving fibrosis in almost one-quarter of recipients. The treatment also shows significant improvements in other histological markers of NASH, including lobular inflammation and hepatocellular ballooning.
The ATS Foundation/Boehringer Ingelheim Pharmaceuticals, Inc. Research Fellowship in Idiopathic Pulmonary Fibrosis aims to advance understanding of the disease through single cell transcriptomic analysis.
A new study from The Westmead Institute for Medical Research identified a genetic variant associated with liver fibrosis in chronic hepatitis C patients. This finding is crucial for preventing health complications and reducing the number of patients requiring liver transplants.
Researchers at VUMC and TGen are studying Idiopathic Pulmonary Fibrosis (IPF), a progressive and irreversible lung disease affecting 50,000 Americans annually. The grants will help identify specific gene expression changes driving the disease, potentially leading to earlier diagnosis and more effective treatments.
A study found that a protein associated with cancer growth is linked to idiopathic pulmonary fibrosis, a chronic and progressive lung condition. Introducing normal cells to inhibit the protein PD-L1 may reduce disease severity in laboratory mice and human tissue samples.
Researchers discovered that inhibiting the cancer-causing protein EZH2 can correct increased fibrosis and abnormal blood vessel function in scleroderma patients. This breakthrough suggests that existing EZH2 inhibitors could be repurposed to treat scleroderma, offering new hope for this currently incurable disease.
Fibrosis, a major complication of butterfly syndrome, is driven by the protein TSP1 and its activation of TGF-beta signaling. Researchers have identified a potential treatment by inhibiting TSP1, reducing fibrosis in tissue-engineered models.
A molecular network controlling connective tissue deposition has been decrypted, revealing a key protein PU.1 that causes pathological scarring. Inhibiting PU.1 may provide a new way to treat fibrotic diseases such as systemic sclerosis and idiopathic pulmonary fibrosis.
In connective tissue diseases, excessive activation of connective tissue cells leads to hardening and scarring within organs. The discovery of the protein PU.1 reveals a molecular mechanism responsible for ongoing activation of these cells, leading to fibrotic diseases.
A new study identifies key factors involved in cell cycle arrest and illuminates a novel intracellular structure, paving the way for new therapeutic targets to treat kidney fibrosis. The research team found that blocking the formation of TASCCs reduced the severity of kidney fibrotic disease progression in preclinical models.
A new study published in Nature Immunology has identified a new type of immune cell that infiltrates lung tissue and initiates fibrosis in idiopathic pulmonary fibrosis (IPF). The researchers were able to prevent fibrosis in mouse models by targeting these cells for destruction, which may lead to new treatments for this terminal illness.
A team of researchers has discovered a potential method to treat radiation-induced skin fibrosis by manipulating metabolism. They found that metabolic abnormalities are a key factor in the development of this condition, and identified several compounds and cell therapy techniques that may help alleviate its symptoms.
A nurse-led specialist clinic in GP surgeries has been shown to diagnose twice as many cases of liver disease than usual care. Simple tests, such as liver stiffness measurements and blood samples, detected nearly half of the patients as having some form of liver disease, including cirrhosis and fatty liver disease.
Researchers at Medical University of South Carolina identify insulin-like growth factor-binding protein 5 (IGFBP-5) as a potential therapeutic target for lung fibrosis. The protein promotes fibrosis by turning on profibrotic genes and increasing levels of profibrotic factors.
Researchers identify strong genetic risk factor for IPF, linking mucociliary dysfunction to lung scarring. The study provides a breakthrough in understanding the cause of IPF and potentially its treatment.
A study found that a gene mutation believed to have protected people from the bubonic plague may also protect HIV patients with hepatitis C from fatal liver scarring. Researchers matched patients with and without the CCR5-delta 32 gene mutation and found that those with the mutation had less fibrosis progression.
Scientists have found a drug combination that can halt the progression of fibrosis, a condition responsible for almost half of all deaths. The study, published in European Urology, tested a combination of phosphodiesterase type 5 inhibitors and selective oestrogen receptor modulators on cells and animals.
Researchers have discovered interleukin IL-22 as a new target to inhibit the progression of liver disease and prevent cancer. The study reveals how IL-22 accelerates fibrosis during chronic hepatitis by amplifying the signal of the fibrogenic cytokine TGF-β.
Fibro-adipogenic progenitors (FAPs) have multiple identities during muscle regeneration, driving symptoms of Duchenne muscular dystrophy (DMD). Targeting FAPs with defined markers may prevent fibrosis and promote regeneration.
A new test predicts advanced fibrosis in NAFLD patients, accurately identifying 92% of those at risk. The tool uses the PRO-C3 biological marker and combines it with clinical information for highly accurate results.
Researchers at the University of Arizona College of Medicine - Tucson are studying two potential drug candidates to stop and reverse excessive scar tissue growth in the lungs. The compounds target the enzyme Nox4, which is believed to be the cause of excessive scar tissue growth.
A new international guideline has been developed to aid in the diagnosis of idiopathic pulmonary fibrosis (IPF), a rare and often fatal lung disease. The guidelines provide evidence-based criteria for diagnosis and recommend multidisciplinary discussions to facilitate accurate diagnosis.
In scleroderma, IL-6-producing effector B cells promote fibrosis, while IL-10-producing regulatory B cells suppress inflammation. Administering a BAFF antagonist selectively depletes Beffs while sparing Bregs, suggesting this approach could be a therapeutic strategy for SSc.
Endurance athletes show more left atrial fibrosis than non-athletes, with the condition linked to a higher risk of arrhythmias and atrial fibrillation. The study suggests that increased left atrial fibrosis may help explain the higher incidence of arrhythmias in endurance athletes.
A study found that progressive massive fibrosis cases among US coal miners rose by 31.5% annually between 1996-2016, defying expectations given improved dust control measures. The increases were highest in Virginia and Kentucky.
IPF is associated with increased extracellular vesicles that relay WNT5A signals to lung cells, leading to scarring and impaired lung function. The study proposes a pharmacological biomarker and therapeutic approach to address this disease.
A new Northwestern Medicine study identified a trigger for some fibrotic diseases and an experimental compound to treat it. The compound, T53, reversed abnormality in three different mouse models of fibrosis, suggesting a novel approach to treat the disease.
A recent study published in eLife discovered that altered collagen structure leads to tissue stiffness during lung fibrosis progression. The researchers identified a compound that blocks LOXL enzymes, which can prevent tissue stiffening and limit fibrosis. This finding suggests new treatment approaches for lung fibrosis.
Researchers at the University of Alabama at Birmingham have shown that metformin can reverse established lung fibrosis using a drug treatment targeting cell metabolism. The study used human lung fibroblasts and a mouse model of lung fibrosis, finding that metformin accelerated the resolution of well-established fibrosis.
A TGen-led study has identified significant gene expression patterns associated with obesity-related NASH inflammation and fibrosis. The researchers discovered 176 genes specific to fibrosis, revealing three cellular pathways and 16 previously associated genes.
Researchers developed a new ultrasound technology, time-harmonic elastography, to diagnose liver fibrosis in obese adolescents without invasive biopsies. The technology accurately distinguishes between patients with no or mild fibrosis and those with moderate or advanced fibrosis.
Researchers from Brigham and Women's Hospital identify NEDD9 as a critical player in disease development, with potential therapeutic implications for patients with PAH. The study found that increased oxidant stress modifies an amino acid residue in NEDD9 to cause lung artery fibrosis.
A new biotechnology, lung-on-a-chip, has been developed to simulate pulmonary fibrosis, a serious lung disease. This innovation could streamline the drug-testing process, making it quicker and less expensive.
Researchers created a 'quick and robust' blood test that can detect liver fibrosis, the first stage of liver scarring, from a blood sample in 30-45 minutes. The new method uses polymers coated with fluorescent dyes to bind to blood proteins, offering a simple and inexpensive way to diagnose disease.
A study from Michigan Medicine discovered that blocking a gene called FOXM1 can reduce the development of fibroblasts and fibrosis in IPF patients. The research used siomycin, an experimental compound designed to block FOXM1, which prevented fibrosis in mice with lung disease.
Researchers have discovered that increasing lipid production in the lungs can reduce lung scarring by 70-80 percent. The study's findings suggest that failing to produce lipids due to injury or age-related metabolic changes may contribute to lung fibrosis development.
Boston University researcher Michelle T. Long has received a five-year, $1 million NIH grant to continue her research on non-alcoholic fatty liver disease (NAFLD). Her study will focus on the clinical and genetic traits associated with hepatic fibrosis in 3,500 participants.
A new study by Hospital for Special Surgery researchers suggests that plasmacytoid dendritic cells play a key role in causing fibrosis and inflammation in scleroderma patients. The study's findings, published in Science Translational Medicine, also identify a potential target for treatment: the TLR8 receptor on the surface of these cells.
Researchers at Max Planck Institute found reduced FoxO3 activity reprograms connective tissue cells, leading to pulmonary fibrosis. Boosting FoxO3 activity halted disease progression in mice, offering a potential treatment pathway.
A Yale-led study shows that thyroid hormone therapy significantly resolves fibrosis in the lungs of mice, leading to increased survival. The researchers found that normalizing mitochondria function in epithelial cells protects them from damage and allows resolution of fibrosis.
Researchers discovered that RAGE protein plays a crucial role in repairing DNA damage and healing tissue in the lungs. Treatment with RAGE protein reversed scarring and restored functionality in mice with pulmonary fibrosis. The study provides new insights into molecular therapy for lung damage and offers potential therapeutic benefits.
Researchers at Technical University of Munich discovered that lower levels of microRNA 29 suppresses cardiac fibrosis, contradicting previous studies. The study highlights potential new approaches for developing drugs against fibrotic diseases, particularly in treating cardiac fibrosis.
Research found that male triathletes are more likely to develop myocardial fibrosis, a scarring of the heart, due to excessive exercise. The study also showed that female triathletes were less prone to the condition.
Researchers at MGH and UHN discovered a critical molecular pathway that induces lung and skin fibrosis in a mouse model. Suppressing ephrin-B2 expression blocked the development of lung fibrosis, while inhibiting ADAM10-sEphrin-B2 signaling reduced fibrosis and death.
Scientists at Duke-NUS and National Heart Centre Singapore have made a major breakthrough discovering that interleukin 11 is responsible for fibrosis and causes widespread organ damage. This finding has the potential to transform treatment of millions worldwide, as inhibiting IL11 can prevent heart and kidney fibrosis.