Articles tagged with Hepatocytes
Researchers found that GSTM3 knockdown promotes liver fibrosis reversal through the inhibition of hepatic stellate cell activation via PPARγ signaling. GSTM3 levels were negatively correlated with reversal, suggesting its potential as a diagnostic biomarker.
A new study reveals that hepatocytes release soluble Tim-3 protein to limit immune-mediated damage in response to drug-induced liver injury. The protein binds to Galectin-3 and Galectin-9 to regulate immune cell infiltration, providing protection against subsequent damage.
Steatotic donor livers are susceptible to post-transplant dysfunction due to galectin-3 (LGALS3)-mediated pyroptosis. LGALS3 modulates NLRP3 inflammasome activity by regulating its ubiquitination, exacerbating graft injury.
A Salk Institute study identifies Fibroblast Growth Factor 1 (FGF1) as the molecular signal that tells the liver when to release fat into the bloodstream, following a precise rhythm timed to the body's internal clock.
Elevated uric acid promotes liver damage and disease severity through inflammation, oxidative stress, and metabolic disturbances. Lifestyle interventions, medications, and potential biomarkers are being explored to improve diagnostic efficacy and treatment.
Engineered tissue grafts can take on the liver's function and help patients with liver failure. The injected cells remain viable in the body for at least two months, generating enzymes and proteins like normal hepatocytes.
A new HepaRG human hepatocyte model with enhanced CYP2D6 activity has been developed to predict drug-induced liver injury. The model enables more human-relevant evaluation of drug toxicity mediated by CYP2D6, offering a promising alternative to animal testing.
A study published in eGastroenterology reveals that Autophagy Related 14 (ATG14) plays a critical role in protecting the liver against injury and fibrosis. ATG14 deficiency leads to severe hepatocellular injury, oxidative stress, and inflammation, highlighting its importance in maintaining hepatocyte homeostasis.
Researchers create detailed 3D reconstructions of human liver tissue, comparing healthy and cirrhotic livers, showing dysregulation of metabolite transport, reduced specialized cells, and disruption of vascular networks. The study highlights the importance of understanding organ structure for bioprinting artificial organs.
Researchers have identified an effective strategy to reduce structural liver damage and improve hepatic vascular function in cirrhosis. Blocking the PAF-R receptor can help rebalance immune and inflammatory responses within the liver.
Researchers used single-cell transcriptomics to study liver injury and repair. They found that hepatocytes can migrate to damaged areas, and that hepatic stellate cells play a dual role in contributing to fibrosis and supporting regeneration. Endothelial cells regulate regenerative signaling, and macrophages exhibit heterogeneity durin...
A study published in the Journal of Hepatology reveals that only 15-20% of neonatal liver cells are responsible for generating over 90% of the adult liver mass. This finding has major implications for pediatric gene therapy, allowing scientists to achieve more effective and durable correction of inherited liver diseases.
Researchers have identified a gene signature indicative of hepatic ferroptosis using an iron overload-induced mouse model and validated it in human liver injury systems. The study highlights the role of ferroptosis in liver injuries and offers potential therapeutic targets.
A study by Toho University researchers reveals a cellular communication network that promotes liver fibrosis. FGF18 and osteopontin enhance the production of OPN, which activates quiescent stellate cells to propagate fibrotic activity. This discovery highlights the critical roles of these molecules in driving liver fibrosis.
Researchers investigated the therapeutic mechanisms of ursolic acid on metabolic dysfunction-associated steatotic liver disease. Ursolic acid was found to reduce inflammation by modulating estrogen conversion via HSD17B14, a crucial enzyme regulating estrogen balance.
This study found that inhibiting cyclooxygenase-2 reduces liver ferroptosis and fibrosis by upregulating the Nrf2 signaling pathway. COX-2 inhibition also restored antioxidant defenses in hepatocytes, reducing oxidative stress and lipid peroxidation.
A team of Chinese researchers identified a novel intercellular signaling mechanism between adipocytes and hepatocytes in endoplasmic reticulum stress response. The study reveals that ceramide, a fat molecule, plays a key role in activating the unfolded protein response pathway in hepatocytes.
Researchers have discovered a previously unknown mechanism of liver regeneration triggered by glutamate, which accelerates liver regeneration in minutes through changes in macrophage metabolism. Hepatocytes producing glutamine synthetase play a key role in this process.
Researchers discovered that PCSK9 and APOA4 are key regulators of TMAO-induced cholesterol metabolism, leading to gallstone formation. Targeting these genes may be a promising approach for preventing and treating cholelithiasis.
The study highlights the significant protective role of Asah1 in preventing NAFLD progression by regulating hepatic lipid homeostasis and cellular maintenance processes. The findings suggest that targeting Asah1 expression or activity may inform new therapeutic strategies for improving patient outcomes.
SLC transporters contribute to the development of hepatic steatosis by regulating lipid metabolism, particularly with SLC2A2, GLUT4, and GLUT5. These proteins influence processes like de novo lipogenesis and insulin resistance in hepatocytes.
Ursodeoxycholic acid (UDCA) exhibits a broad range of hepatoprotective mechanisms, including antioxidant, anti-inflammatory, and anti-apoptotic properties, which may benefit various types of drug-induced liver injury. In hepatocellular DILI, UDCA reduces inflammation, alleviates ER stress, and protects against mitochondrial damage. In ...
The Rice University lab, in collaboration with Baylor College of Medicine, has developed a new gene-editing strategy called Repair Drive that improves the effectiveness of gene therapies in the liver. The technique enables the repair of liver cells at higher rates and equips them with a selective advantage to outcompete incorrectly edi...
Researchers reveal senescence's impact on liver health, from repair and regeneration to chronic disease progression. Emerging therapies, such as senolytic treatments, aim to selectively eliminate senescent cells while preserving healthy tissue.
Overexpressing hepatic SLC7A11 leads to glutamate and serine deficiency, promoting MASLD progression through ferroptosis. Serine supplementation rescues the disease phenotype.
Researchers at UNC Health Care have discovered a little-known protein, PDGFA-associated protein 1 (PDAP1), that plays a crucial role in the replication and infection of hepatitis A virus. The protein is used by the virus to exploit the host cell's stress response, allowing it to produce its own proteins necessary for replication.
A new co-culture system uses photosynthetic microorganisms to remove waste products and enhance muscle cell growth, resulting in a 30% reduction of lactate and over 90% reduction of ammonia. This innovation provides a low-cost, sustainable alternative to animal serum for cultured meat production.
A 48-week follow-up study found that TMF treatment did not significantly affect blood lipid profiles in patients with chronic hepatitis B. Lipid indices remained stable, regardless of baseline characteristics.
Researchers identified CYP1B1 as a biomarker for HSC activation and liver fibrosis in patients and mice. Inhibition of CYP1B1 led to the accumulation of trehalose, which has anti-fibrotic activity, protecting mice from liver fibrosis.
Cancer cells can attach themselves to liver cells when specific proteins are present, allowing them to colonize and form new tumors. This discovery provides insights into the metastatic process and may lead to potential treatments that prevent cancer from establishing new tumors.
Autoimmune liver diseases like AIH, PBC, and PSC exhibit distinct cellular targets and inflammatory profiles. Single-cell RNA sequencing and spatial transcriptomics provide new insights into their pathogenesis and potential treatment strategies.
A team of researchers has discovered a mechanism by which the liver's immune cells are suppressed in chronic hepatitis B, leading to organ damage. The 'sleep timer' function allows immune cells to weaken their activity over time, preventing them from proliferating excessively and causing further damage.
This study found that TIMP-1 induces the expression of transcription factor Fli-1, which elevates MCP-1 expression and promotes hepatic macrophage recruitment. siRNA-TIMP-1 alleviated liver fibrosis by reducing macrophage migration and MCP-1 expression.
Researchers developed an ex vivo gene-editing protocol to treat hereditary tyrosinemia type 1 using liver cell therapy. The study showed robust engraftment and expansion of transplanted gene-edited hepatocytes in recipient mice, correcting disease indicators such as normalized tyrosine, phenylalanine levels.
Researchers have developed a novel patch that can help liver tissue regenerate and inhibit inflammation. The patch demonstrated restored liver function in lab tests and promoted recovery from liver fibrosis in rats, showing great potential for treating liver diseases.
Human umbilical cord mesenchymal stem cells (hUC-MSCs) have been shown to alleviate acute liver failure by inhibiting hepatocyte apoptosis and regulating macrophage polarization. This study suggests that hUC-MSC-based cell therapy may serve as an alternative option for patients with liver failure.
Researchers have successfully grown functional human liver cells in a different species, offering a potential solution to the shortage of donor organs for liver transplants. The breakthrough uses interspecies blastocyst complementation to produce transplantable human liver cells, which can effectively mitigate chronic liver fibrosis.
Researchers at UW–Madison developed a method using short electric pulses to increase gene therapy material uptake in liver cells, reducing dosage needed. The technique could help treat genetic diseases like cystic fibrosis and sickle-cell disease.
A study from Medical University of Vienna reveals a new molecular signaling pathway crucial to liver cancer development, offering potential new therapeutic targets. The research also identifies the c-Jun/Fra-2 complex as essential in triggering tumour growth.
Researchers discovered that liver cells secrete SAA proteins, which hinder T cell infiltration and attack tumors. Deleting SAA proteins increased survival times and likelihood of cures in mice with pancreatic tumors.
Research reveals that FoxO6 upregulates ApoC3, leading to increased lipid accumulation and liver damage in aged rats on a high-fat diet. The study suggests that targeting this pathway may offer therapeutic strategies against hepatic steatosis.
The study reveals that a gene called mTOR, which works like a GPS, directs the specialization of liver cells according to their position. After birth, the fluctuation in nutrient supply triggers the activation of this gene, completing the maturation of the liver.
Researchers investigated the molecular mechanism of serum iron overload-induced BMP/SMAD pathway and hepcidin expression. SMURF1, a master regulatory function, mediates Holo-Tf-induced SMAD1/5 activation and hepcidin expression. The inhibition of SMURF1 may represent a therapeutic strategy for iron overload-related diseases.
Research reveals oestrogen's protective role in preventing fatty liver disease by targeting the TEAD1 protein. The discovery could lead to a new treatment for fatty liver and liver cancer, as well as earlier detection methods.
Researchers at Karolinska Institutet developed a method to study liver function and disease using the cornea of mice eyes. They transplanted liver cells into the eyes, creating a non-invasive platform to monitor liver health over time.
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 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.
Researchers developed a new technology to test new drugs against liver diseases by recreating the real human liver environment. The model consists of live liver cells in an artificial blood vessel system, allowing for controlled testing and monitoring.
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.
A nationwide study from Karolinska Institutet in Sweden found that close relatives and partners of people with metabolic-associated fatty liver disease (MASLD) are at a higher risk of developing liver cancer and severe liver disease. This suggests that family members could benefit from the same lifestyle advice as patients with MASLD.
High pressure in bile canaliculi alters liver tissue structure, leading to the formation of liver cell rosettes observed in various liver diseases. The study identifies pressure as a potential cause of biliary obstruction-related diseases.
Researchers developed a liver-targeting drug that reversed obesity and lowered cholesterol in obese mice by delivering the drug via nanogel. The treatment, which was administered intraperitoneally, effectively normalized weight and reduced cholesterol levels despite continued high-fat diet consumption.
A new nanogel-based carrier delivers a synthetic thyroid hormone mimick to liver cells, resulting in weight loss and improved cholesterol levels. The treatment also resolves liver inflammation with minimal side effects, offering potential for other liver-based diseases.
Researchers developed new methods for detecting drug-induced hepatotoxicity using 3D cell cultures and mass spectrometry imaging, identifying biomarkers and effective interventions. A zeolite-based protein corona method was also used to characterize plasma proteins, enabling the identification of low-abundance proteins and their potent...
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.
Researchers investigated premature senescence in biliary atresia and assessed senotherapies. They found that human allogenic liver-derived progenitor cells reduced early markers of senescence and improved liver disease in a preclinical model, providing encouraging results for pediatric biliary cirrhosis treatment.
Researchers have developed biodegradable hollow nanoscavengers that target reactive oxygen species to restore liver function and reverse insulin resistance in human liver cells and diabetic mice. This innovative approach offers a promising pathway toward long-term treatment of type 2 diabetes and other metabolic diseases.
A study by researchers at TUM found that gut bacteria play a crucial role in liver regeneration. The microbiome produces short-chain fatty acids, which are essential for liver cell growth and division. In mice treated with antibiotics, liver regeneration was delayed or not possible, but a
Researchers found that P2-HNF4α expression is associated with p-STAT3 and c-Myc expression in NAFLD patients, suggesting potential biomarkers for hepatocellular carcinoma (HCC) risk. Additionally, p-STAT3 expression was linked to hypertension, while c-Myc expression was associated with advanced fibrosis.
Comprehensive metabolic changes convert mature liver cells into immature progenitor cells that proliferate rapidly and develop tumors. The main causes of liver cancer are metabolic disorders and infections with hepatitis C virus and high alcohol consumption.