Articles tagged with Fibrosis
Researchers found a three-component signaling pathway in hepatic stellate cells that leads to collagen production and liver fibrosis. A novel RNA-based treatment, ASO, was designed to block this pathway, preventing fibrosis without side effects.
Researchers developed a new experimental strategy to tackle scarring and fibrosis by releasing enough collagen to prevent tissue damage while protecting it from excessive amounts. The strategy, which uses molecules known as peptides to block the export of collagen from cells, shows promise in treating conditions such as scleroderma.
Researchers at Michigan Medicine discovered a pathway that reverses idiopathic pulmonary fibrosis (IPF), a common type of lung scarring. The study found that inhibiting the molecular brake MKP1 is essential for spontaneous resolution of fibrosis, offering new hope for patients with IPF.
A team of researchers at Weill Cornell Medicine has discovered a critical protein sensor called SEL1L that regulates collagen clearance from tissue. This finding provides new insights into the development of therapeutic strategies for diseases like lung fibrosis, which currently have no effective treatments.
Research reveals a dynamic pattern of gene expression in liver fibrosis, with persistent effects even during regression. The study identifies key 'hub' genes that could be developed into biomarkers for future therapies.
Researchers at UVA Health discovered a potential blood test to predict patients with severe COVID-19 who are likely to recover well and those at risk of long-term lung problems. The study found that patients with late-resolving symptoms had fewer immune cells in their blood, correlating with symptom severity.
Researchers used generative AI to design a lead molecule for treating fibrosis, a biological process associated with aging. The compound, INS018_055, demonstrated significant efficacy in preclinical studies and showed promising results in clinical trials, accelerating drug discovery and providing new therapeutic options.
A new computer model of a human lung is being used to simulate the interaction of radiation with lung tissue at a cellular level. This could lead to more targeted treatments for cancer and reduce damage caused by radiotherapy.
Researchers at NDORMS identified how cells work to resolve frozen shoulder, opening up potential new targets for treatment. The study found that distinct populations of macrophages in the shoulder capsule promote tissue remodelling and reduce inflammation.
A VUB research team has identified a specific protein, GPR176, that contributes to liver fibrosis. The discovery opens up possibilities for developing new drugs to treat this condition.
Research from the German Cancer Research Center reveals that repetitive changes in female reproductive organs over time lead to chronic inflammation and fibrosis, which may contribute to increased uterine cancer risk. The study mapped the effects of estrous cycle, pregnancy, and aging on the reproductive tract.
A new study found that one bacterial species, Streptococcus mitis, dominates in IPF patients not treated with antibiotics and is associated with better lung function and survival. This protective relationship does not apply to patients who received antibiotics.
Researchers at University of Virginia Health System developed a new approach to machine learning that identifies drugs minimizing harmful scarring after heart attacks. The tool predicts and explains drug effects for other diseases as well.
A new 3D bioprinted liver tissue model has been developed to study nonalcoholic steatohepatitis (NASH), a serious complication of nonalcoholic fatty liver disease (NAFLD). The model, created using liver cells from healthy or NASH-diseased donors, displays all characteristics of the disease, including fibrosis.
A groundbreaking study identifies FAM3C as a key regulator of breast cancer progression within the tumor microenvironment. The overexpression of FAM3C promotes breast cancer cell survival and metastasis, while its depletion inhibits tumor growth in genetically engineered mouse models.
The University of Rochester is establishing a new NIH-funded center focused on developing FDA-qualified drug development tools related to barrier functions in disease. Researchers will create microphysiological systems with ultrathin membranes of human cells, aiming to reduce animal trials and improve drug efficacy.
A new technique, CLivD score, has been developed to improve liver fibrosis treatment. The study found that the CLivD score can identify at-risk individuals, reducing the need for further evaluation and streamlining screening. This approach holds promise for early detection of liver disease and preventing complications.
Researchers found that higher levels of omega-3 fatty acids in the blood plasma were associated with better lung function and longer survival without needing a lung transplant. This was consistent regardless of smoking history or cardiovascular disease.
Researchers at IRB Barcelona discover iron accumulation as a driver of pathological senescence and fibrosis, highlighting its role in various fibrotic disorders. The study identifies potential methods for non-invasive assessment and treatment of fibrotic diseases via MRI and chemical compounds.
Researchers discovered that RvD2, a specialized proresolving lipid mediator, can alleviate established liver scarring or fibrosis. Treatment with RvD2 improved liver histopathology and increased bone marrow and blood monocytes.
Duke-NUS scientists have discovered a universal pattern in macrophages that form scars across various organs. They found two groups of macrophages with opposing roles: one promoting fibrosis and another dismantling it, which could lead to new therapies for fibrotic diseases.
Researchers found intestinal hormones can inactivate liver's star-like cells responsible for scar tissue formation. This discovery could lead to new treatments targeting cell changes, avoiding severe side effects.
Researchers have made significant progress in understanding a pathway contributing to liver fibrosis. Paxillin has been found to play a key role in the activation of hepatic stellate cells, leading to excessive extracellular matrix production and scarring. This discovery holds promise for developing new treatments for liver fibrosis.
Researchers found a total of 4,721 proteins altered with age in the murine ovary, including upregulated ECM proteins associated with fibrosis. Age-dependent changes also affect immune response pathways and unique immune cell populations.
A new study reveals FGF18 as a key inducer of hepatic stellate cell proliferation and liver fibrosis. FGF18 levels are dramatically elevated in fibrotic livers, and its overexpression induces liver fibrosis in mice.
A University of Virginia team has developed a new analytical tool using hydrogels to cultivate vascular sprouting from mouse lung tissue, providing new insight into idiopathic pulmonary fibrosis. The research aims to understand the biomechanical and biochemical cues to blood vessels in the lungs during disease progression.
Five lung stem cell variants dominate CF lungs, causing inflammation, fibrosis, and mucin secretion. CFTR modulators fail to suppress these inflammatory variants, suggesting they as key targets for new drugs.
Researchers at Boston University School of Medicine have identified abnormal interactions between platelets and immune cells that promote lung fibrosis. Blocking histones using antibodies alleviated the disease, providing novel mechanistic insights into its development.
A new study found that living donor liver transplant access optimizes the timing of transplant for older, frail cirrhosis patients. Patients with moderate to severe frailty, short stature, and low MELD scores benefited from LDLT, reducing waitlist mortality and improving post-transplant outcomes.
Researchers at Nagoya University developed a unique supramolecule to remove cholesterol from macrophages, stopping the development of non-alcoholic steatohepatitis (NASH) in mice. Cholesterol crystals are also found in human patients, suggesting a potential therapeutic strategy.
Researchers aim to identify genetic risk factors and mechanisms underlying virus-induced asthma, using artificial intelligence-based techniques and patient-derived models. The study may lead to personalized prevention campaigns and mechanism-targeted drugs.
Liver fibrosis development is driven by various factors, including metabolic syndrome and insulin resistance. CD8+ T cells play a significant role in activating hepatic stellate cells, which produce scar tissue.
Researchers found that human senescent fibroblasts trigger progressive lung fibrosis in immunodeficient mice by inducing paracrine senescence and pro-fibrotic activities. The study also suggests that senolytic compounds like navitoclax can ameliorate lung fibrosis induced by senescent human fibroblasts.
A study published in Hepatology reveals that abnormal pre-mRNA splicing is associated with liver disease caused by excessive alcohol consumption. The researchers propose targeting specific splicing factors as a novel approach to mitigate the disease.
Extracellular vesicles from fibrotic lungs can activate dormant fibroblasts in healthy lungs, initiating fibrosis development and spreading. The study's findings support the potential use of EVs as a targeted drug therapy platform to slow fibrosis progression and improve patient outcomes.
Researchers have identified a potential new drug that improves both liver fibrosis and inflammation in patients with nonalcoholic steatohepatitis (NASH). The drug, Pegozafermin, mimics the body's natural hormone FGF21, controlling energy use and lipid metabolism in the liver.
A novel imaging agent has been developed to non-invasively detect pulmonary fibrosis in its early stages. The agent targets extracellular matrix fibers and has shown significant uptake in lungs with pulmonary fibrosis, matching histological results. This breakthrough could lead to earlier detection and better monitoring of the disease.
Researchers developed a more accurate model of human cardiac fibrotic tissue, which could enable quicker drug testing and potentially lead to new therapies for heart failure. The model, built using an electrospinning technique, recreates the unique aspects of scarred cardiac tissue.
Researchers found a link between short telomeres in ATII cells and lung fibrosis in post-COVID-19 patients. The study revealed loss of ATII cellularity and shorter telomeres concomitant with increased fibrotic lung parenchyma remodeling.
Research identifies Indian Hedgehog protein as a key driver of chronic kidney disease and heart damage, offering new hope for treatments. The findings suggest that blocking the protein's actions could improve kidney function and reduce cardiovascular risk.
Researchers found variant cells in lungs of IPF patients that can drive fibrosis and inflammation. These cells may be targeted for future therapy, offering new hope for treatment.
Researchers discover that senescence-associated secretory phenotype (SASP) can induce neuroendocrine transdifferentiation (NED) in breast cancer epithelial cells, promoting tumor progression and aging-related features. SASP's dual role in cancer involves both antitumoral and tumorigenic effects.
Vogel and Benn's study replicates tissue growth in vitro, revealing the importance of ECM interactions. Myofibroblasts play a key role in wound healing and cancer progression, but their transformation into fibroblasts is influenced by ECM composition and structure.
This study examined the effects of deferoxamine and ferrostatin-1 on salivary gland dysfunction in ovariectomized rats. The researchers found that these compounds reduced inflammation, fibrosis, and improved salivary gland function, suggesting potential treatments for postmenopausal xerostomia.
Researchers discovered ERK signalling is a crucial switch between scarring and regeneration, with prolonged activation promoting regenerative success. Modulating ERK activity could potentially stimulate regeneration in clinical settings.
A new study published in The Lancet shows that metabolic surgery is more effective than medications and lifestyle interventions in treating advanced non-alcoholic fatty liver disease. The trial compared three active treatments and found that surgery reversed inflammation and improved liver fibrosis, leading to better overall health ben...
Researchers have discovered that manipulating Yes-associated protein (YAP) expression in liver progenitor cells can improve their ability to regenerate and repair liver tissue. This could lead to new treatments for chronic liver diseases.
Small vesicles released by intestinal bacteria induce immune activation and progression of liver cirrhosis, as well as reduction of serum albumin level, leading to edema and ascites in patients with cirrhosis.
The American Roentgen Ray Society presents its 2023 Honorary Lecture on Advanced High-Resolution CT, dedicated to the late Dr. W. Richard Webb, who transformed thoracic imaging with his foundational work in HRCT. The lecture explores multiple conditions diagnosed via HRCT and the radiologist's role on multidisciplinary teams.
A study by University of Rochester Medical Center researchers reveals how a biological clock molecule contributes to lung scarring. Low levels of REV-ERBα have been linked to increased collagen production and worse lung damage in patients with pulmonary fibrosis.
Human macrophages use Siglec-14 receptors to recognize and engulf carbon nanotubes, leading to inflammation. The discovery could pave the way for developing safer carbon nanotubes and therapies to prevent inflammatory diseases.
Researchers at TUM have developed a method to create mini-hearts in Petri dishes using stem cells. The resulting organoids mimic the earliest stages of human heart development and can be used to investigate congenital heart defects, potentially leading to new treatment methods.
Scientists have identified an autoinflammatory disease called Lyn kinase-associated vasculopathy and liver fibrosis (LAVLI) linked to mutations in the LYN gene. The research suggests that Lyn kinase may be a potential therapeutic target for drugs treating non-syndromic small vessel vasculitis and inflammation-induced liver fibrosis.
A study published in Cell Death & Disease reveals that a protein cross-linking enzyme called TG2 exacerbates kidney fibrosis by polarizing M2 macrophages. The researchers hope to develop treatments for diseases caused by inflammation imbalance, such as fibrosis, cancer, and atherosclerosis.
Researchers from Kyushu University found that the single mechanosensitive protein VGLL3 induces fibrosis, thickening and scarring tissue. The study suggests targeting this protein could lead to new treatments against fibrosis.
Researchers found that senescence-associated exosomes (SA-EXOs) from MSCs induce fibrosis and activate invasive characteristics in neighboring cells via the TGF-β pathway. SA-EXOs play a large role in cancer-related fibrosis, and their unique miRNA content influences myofibroblast phenotypes.
Researchers discovered that lipid deposition on medical implant surfaces can signal to the immune system whether to attack or ignore the implant. This knowledge could help develop biomaterials that deflect host immune aggression, reducing malfunction rates for devices like pacemakers and surgical mesh.
A new study found that Black patients with pulmonary fibrosis are significantly younger than their Hispanic and white counterparts, experiencing accelerated disease progression. Lifestyle and socioeconomic factors linked to environmental exposures may contribute to these disparities.
Researchers at Mass General Hospital have found that intestinal fibrosis plays a critical role in the progression of inflammatory bowel disease (IBD), affecting the growth and differentiation of intestinal stem cells. The study suggests targeting mechanosensing pathways may offer an attractive therapeutic strategy for IBD.
A study published in Radiology revealed persistent lung abnormalities in patients two years after COVID-19, including fibrosis and cystic changes. The incidence of lung abnormalities gradually decreased over time, but the proportion of fibrotic interstitial lung abnormalities remained stable.