Articles tagged with Fibrosis
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.
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.
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.
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.
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.
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.
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.
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 ...