Extracellular vesicles (EVs) are key players in the pathogenesis of chronic lung diseases, modulating cellular senescence and immune-inflammatory responses. EVs facilitate aberrant intercellular communication, deliver pathogenic miRNAs and proteins, and promote chronic inflammation.
Researchers at Sanford Burnham Prebys discovered that blocking an energy transfer enzyme shifts mammalian hearts into a regenerative state, promoting regeneration and improving recovery after a heart attack. By modulating heart cell metabolism, scientists can potentially awaken the heart's dormant regenerative abilities.
Researchers at Memorial Sloan Kettering Cancer Center have developed nanoparticles that can selectively eliminate a small population of immune cells found to drive fibrosis, potentially paving the way for new approaches against immunotherapy-resistant tumors and fibrotic diseases. The approach could make immunotherapy work for more pat...
Researchers found that post-transplant cirrhosis cases often reflected recurrence of the original disease, with lower long-term survival rates. The study highlights the need for lifelong surveillance of fibrosis progression after transplantation to improve outcomes.
Insilico Medicine has dosed the first patient in the GENESIS-IPF-3 Phase III clinical trial of Rentosertib, a generative AI-driven innovative drug for idiopathic pulmonary fibrosis. The 52-week trial aims to evaluate Rentosertib's efficacy and safety in a larger cohort of patients with IPF.
Researchers at Cedars-Sinai Medical Center tested a novel drug called TY1, which targets an immune system pathway, and found it reduced inflammation and DNA damage in immune cells. The drug also improved heart function and physical activity in laboratory mice with a condition mimicking systemic sclerosis, suggesting a potential future ...
Researchers found that corisin, a bacterial protein fragment, drives tissue fibrosis by disrupting the cell's quality-control system. Antibody treatment can help by blocking corisin, demonstrating its biologically active and causally supported role in disease.
Txn1 mutant rats exhibit severe kidney deterioration, with hallmarks of human CKD, including oxidative stress, mitochondrial dysfunction, and inflammation. The study identifies a link between chronic thioredoxin deficiency and CKD progression, suggesting promising therapeutic approaches.
Researchers at Boston Children's Hospital identified a new target responsible for bone marrow scarring in myelofibrosis, a type of blood cancer. Combining traditional therapy with drugs blocking scar formation may improve treatment outcomes. The study found that inhibiting freecycling activity with drugs like hydroxychloroquine can red...
Researchers found that people with well-controlled HIV have more fibrosis in their fat tissues, leading to insulin resistance and type 2 diabetes. The study also identified a blood marker of scarred fat, which may help predict metabolic future for individuals with HIV.
Researchers engineered a biochemical halo of interleukin 10 to suppress immune rejection of pancreatic beta cells, enabling implanted insulin-producing cells to control blood sugar for over 100 days. The approach could lead to a cure for Type 1 diabetes and improve outcomes for implantable therapies.
A University of Virginia researcher received a $2.1 million grant to develop advanced laboratory tissue models that could improve drug testing, deepen scientists' understanding of disease, and reduce the need for animal testing.
Researchers have developed a new biological treatment that targets inflammation-driven scarring after a heart attack, aiming to reduce the risk of heart failure. The treatment uses donated human bone marrow-produced exosomes to dampen inflammation and promote healing.
Researchers found that Bofutsushosan reduced fibrosis in fat tissue and liver of mice with obesity, and identified herbal components with anti-fibrotic activity. The study suggests that Bofutsushosan may have benefits beyond weight control, providing a scientific basis for studying Kampo medicines.
Scientists have uncovered a new mechanism used by heart cells to resist reprogramming and found that carbohydrate sulfotransferase 7 (CHST7) is the most potent preventer of reprogramming in mouse and human cells. By targeting CHST7, researchers may develop treatments to help the heart fix itself after injury.
Researchers identified a key driver of liver fibrosis progression: FSP1+ macrophages that activate PGK1 through lactylation. This self-reinforcing loop amplifies glycolytic signaling, promoting liver fibrosis. A cell penetrating peptide targeting PGK1 lactylation blocks fibrosis progression in preclinical models.
Researchers have identified a protein called vitronectin that triggers the scarring in lungs leading to idiopathic pulmonary fibrosis. This discovery opens up a new potential treatment pathway using the vitronectin-macrophage pathway to inhibit scar tissue growth.
Researchers have found that GLP-1 agonists can normalize genetic pathways involved in pulmonary fibrosis, a lung disease associated with Long COVID. The treatment has shown promise in reducing the risk of fibrous buildup, suggesting potential benefits for people with type 2 diabetes and severe COVID-19 symptoms.
Macrophages are critical drivers of chronic allograft failure, with emerging strategies targeting key macrophage signaling pathways providing an important conceptual shift. Targeted therapies, such as inhibiting the purinergic pathway and mTOR/NF-κB pathway, show promise in preventing chronic rejection.
Researchers found that smoking substantially stiffens human lung parenchyma, making breathing progressively difficult. The study provides detailed mechanical data for human lungs, which may improve ventilator design and surgical planning tools.
A new study published in The Journal of Sexual Medicine found that combining phosphodiesterase type 5 inhibitors with selective oestrogen receptor modulators may slow or stop disease progression when given early. This combination resulted in improved penile curvature and reduced pain during erections compared to standard care.
Researchers identify key mechanism behind age-related persistence of pulmonary fibrosis, revealing disabling collagen clearance due to loss of protein fPRDM16. Restoring fPRDM16 expression rejuvenates fibroblasts' healing function and resolves fibrosis.
Researchers at King's College London uncover a timing mechanism in cells that allows them to ignore brief mechanical stimuli while reacting to sustained changes. This discovery has huge implications for disease treatment and could lead to the development of better therapies for cancer and fibrosis.
The INS001-055 inhalation solution is the world's first AI-driven candidate to receive IND clearance. It targets Idiopathic Pulmonary Fibrosis (IPF) with a novel molecule structure and demonstrates good tolerability, PK profiles, and dose-dependent efficacy trend.
Researchers identified blocking ID1 and ID3 as a promising therapeutic strategy to halt and reverse lung scarring in idiopathic pulmonary fibrosis. The approach showed significant reduction in lung scarring and improvement in lung function across multiple experimental systems.
A recent CNIO study has identified a key mechanism in the development of liver fibrosis by targeting bile duct cells. The research reveals that these cells regulate liver health and form a barrier that prevents bile acid leakage and fibrosis, opening new avenues for personalized treatment.
Researchers investigate whether micro- and nanoplastics contribute to liver disease through oxidative stress, fibrogenesis, and inflammation. They emphasize the need for increased research into plastic-induced liver injury and its potential impact on human health.
A study by IRB Barcelona researchers sheds light on the regulation of protein production in fatty liver cells, revealing a key role for CPEB4 in controlling gene expression. The findings provide new perspectives on the disease and its progression towards more severe forms.
A new study finds that people with metabolic dysfunction-associated steatotic liver disease face a significantly higher risk of liver fibrosis if they engage in episodic heavy drinking. Episodic heavy drinking is defined as four or more drinks for women and five or more drinks for men, at least once a month.
Research reveals that TGF-β1 plays a critical role in fibrotic scar tissue formation, limiting neural regeneration and recovery after spinal cord injury. Inhibiting TGF-β1 signaling reduces fibrotic scarring and improves functional recovery.
A team of researchers at MSU used machine learning to predict how chemicals will influence gene expression, leading to the discovery of promising compounds for the treatment of liver cancer and a chronic lung disease. The study results from years of interdisciplinary work across multiple disciplines and institutes.
Researchers discovered that tendon stem cells and progenitor cells fail to differentiate into mature, functional cells, instead promoting scar buildup. Immune cells, including macrophages, also play a central role in sustaining fibrosis, creating a self-sustaining environment that is difficult to reverse.
Women with cardiometabolic risk factors such as type 2 diabetes and high waist circumference face a higher risk of liver fibrosis, with rates increasing 11-fold and 2.8-fold compared to men. The study highlights the importance of managing these risk factors for liver health beyond heart disease prevention.
Researchers found that an approved antifibrotic drug, finerenone, can reduce ovarian fibrosis and promote follicle growth in women with premature ovarian insufficiency. Clinical trials showed that finerenone improved follicle development and mature oocyte quality in women with POI.
A team of researchers led by Rice University bioengineer Omid Veiseh is developing a first-of-its-kind regenerative treatment aimed at restoring damaged lymphatic vessels and potentially curing lymphedema. The therapy, called ELIXIR, uses engineered human retinal pigment epithelial cells to rebuild broken lymphatic vessels.
A study found that the TF-rs1049296 C>T variant is associated with a higher risk of significant liver fibrosis in patients with MASLD, particularly in those with RES iron deposition. The variant was also linked to increased risk of SF in mixed hepatocellular/RES iron deposition patterns.
Researchers found that activating specific healing pathways in fibroblasts from facial tissues can lead to regenerative wound healing with reduced scarring. This study could lead to new treatments for scar formation and its associated complications, including chronic pain and disease.
Cirrhotic cardiomyopathy involves structural, inflammatory, and metabolic pathologies. Inflammation and mitochondrial dysfunction promote cardiac damage, and the liver-heart axis highlights the impact of cirrhosis severity on cardiac health.
Researchers discovered genes that regulate fibroblast growth, which builds the scaffolding between cells. Adjusting these factors reversed age-related changes and improved health outcomes in mice. The study offers new opportunities to understand and reverse aging-related diseases.
Researchers from Okayama University and Tohoku University have identified a promising way to breach the physical and biochemical barrier created by fibrosis in pancreatic cancer. By blocking collagen signaling through DDR1, they improve drug delivery and enhance treatment response.
Researchers used CRISPR technologies to discover previously unannotated DNA stretches in the 'dark genome', which control cell response to mechanical properties of their environment. This work could lead to new therapeutic targets for illnesses involving changes to tissue mechanics, including fibrosis and cancer.
A study by University of Arizona researchers reveals a previously unknown population of circulating immune cells that play a critical role in fibrosis, the buildup of scar tissue. Blocking signals from these cells during wound healing can reduce scar tissue formation and promote normal healing.
Researchers discovered a dual mechanism by which Oroxylin A inhibits SIRT7, reprogramming HSCs through PRMT5 succinylation-driven senescence and ecto-calreticulin-dependent NK cell immune clearance. This approach provides a promising candidate for anti-fibrotic therapy.
Researchers from Osaka Metropolitan University have discovered that Lawsone, a chemical derived from Lawsonia inermis, can reduce markers of liver fibrosis and promote antioxidant functions in hepatic stellate cells. The study suggests that Lawsone could be used to control and even reverse the effects of fibrosis.
Researchers developed a composite bioabsorbable hemostatic sponge inspired by mussels and extracellular matrix. The sponge quickly absorbs blood and firmly adheres to tissues, enhancing hemostatic performance. It promotes wound stabilization, accelerates blood clotting, and reduces inflammation and tissue damage.
Denis Evseenko and Toby Maher are developing a regenerative drug to block cells that promote fibrosis in the lungs, aiming to slow or reverse IPF damage. The team plans to test the safety and therapeutic potential of their drug-like molecules in animals and human cells.
TGF-β inhibition holds promise for treating liver fibrosis by targeting SMAD-dependent and -independent pathways. Various therapeutic strategies, including direct blockade, receptor inhibitors, antisense oligonucleotides, and natural products from Traditional Chinese Medicine, are being explored to disrupt the TGF-β signaling pathway.
Researchers discovered a mutation in the POT1 gene that prevents telomeres from repairing, leading to pulmonary fibrosis. This study highlights the importance of personalising treatments for diseases caused by dysfunctional telomeres.
Researchers found that shutting down a signaling pathway in fibroblasts restored heart functioning in lab models. The study suggests that targeting fibroblasts may be essential to treat dilated cardiomyopathy, a leading cause of heart failure.
A novel drug target, CD300a, has been identified to suppress immune cell activation and prevent chronic heart and kidney failure after acute tissue injury. The treatment preserves cardiac function and reduces renal fibrosis in mice with genetic deficiency of CD300a.
Penn Engineering researchers used a technique called photochemical cross-linking to stiffen lung tissue, revealing changes in cell behavior that may drive fibrosis. The team observed transitional cells caught in an identity crisis, unable to perform either role well, which contributed to disease progression.
Researchers at Duke University developed a wireless patch that non-invasively measures skin and tissue stiffness, providing real-time feedback for medical applications like wound healing and chronic conditions. The technology also has potential for athletic performance optimization and rehabilitation.
Researchers at Lehigh University and the Cleveland Clinic are developing a nonsurgical therapy for pelvic organ prolapse using drug-delivering nanoparticles. The treatment aims to delay or reverse matrix degradation, reducing the severity of POP in patients with earlier stages of the disorder.
A new investigational drug, ION224, shows promise in treating metabolic dysfunction-associated steatohepatitis (MASH), a serious form of fatty liver disease. By targeting the DGAT2 enzyme, the drug helps reduce fat buildup and inflammation, two major drivers of liver damage.
Researchers found that a molecule produced by gut bacteria can cause inflammation, scarring and fibrosis in the kidneys, a major complication of diabetes. Corisin, a small peptide, attaches to albumin in the blood and targets the delicate kidney structures, accelerating aging and cell death.
Catherine Whittington, a WPI researcher, has received a CAREER Award to develop laboratory models for the study of fibrosis in pancreas, skin, and uterine fibroids. The models will help researchers better understand factors at the cellular level that lead to fibrosis and how interventions can interrupt or reverse it.
Researchers at Texas Biomed have developed a live attenuated vaccine that showed high efficacy in cells and animal models, protecting mice from lethal H5N1. The team identified potential treatment targets using human airway organoids, revealing how bird flu remodels airway cells and causes scar tissue to form.
A substantial proportion of asymptomatic individuals in Greater Vancouver have undetected MASLD and significant fibrosis. Age, male sex, ethnicity, cardiac disease, diabetes, hypertension, and obesity were significantly associated with fibrosis.
The new guidelines introduce a pivotal terminology shift, replacing NAFLD with MASLD and NASH with MASH. MASLD is now grouped under the umbrella of "steatotic liver disease" (SLD), along with alcohol-associated liver disease (ALD) and other causes.
A new study sampled different lung regions in cystic fibrosis patients before and after treatment with modulators, revealing that infections persisted throughout the lungs and drove inflammation. The findings suggest damage may not be the main cause of infection persistence, raising concerns about ongoing lung function deterioration.