Articles tagged with Hepatocytes
A new approach developed by Kyoto University scientists provides insight into the liver stage of the Plasmodium vivax malaria parasite. The method involves infecting human liver cells with mosquito-bred parasites, enabling researchers to study the parasite's life cycle and develop more effective treatments.
Researchers at Boston University and Boston Medical Center have assembled the largest repository of patient-derived stem cells from AATD patients. The cells can be used to study genetic diseases and potentially find new treatment approaches for AATD.
Scientists successfully deliver healthy mitochondrial complexes to liver cells in rats, offering a new approach for treating liver diseases. The method, which uses a protein coating to target mitochondria to the liver, shows promise for addressing a significant gap in current treatments.
Researchers from Kanazawa University discovered SLC35B1 as a crucial molecule in the detoxification process, enabling glucuronidation of drugs and toxicants. The study revealed that SLC35B1 significantly affects UGT activity when knocked down, suggesting its vital role in regulating this complex process.
Researchers at the University of Pittsburgh School of Medicine have created fully functional mini livers using skin cells from human volunteers. The lab-made organs were then transplanted into rats, with results showing they survived for four days and functioned like a normal liver.
Researchers found an unexpected connection between electron imbalance in liver cells and many metabolic problems, including cardiovascular disease and fatty liver disease. The study identified a biomarker, alpha-hydroxybutyrate, to test for reductive stress and suggests LbNOX as a potential treatment.
Gangliosides, sugary fatty acid molecules, are essential receptors for hepatitis A virus (HAV) infection, allowing the virus to enter liver cells. The discovery provides new insights into HAV's unique mode of transmission and opens avenues for antiviral research.
Researchers have made a breakthrough in targeting non-cancerous senescent cells to slow down liver tumor growth. The study, led by Celeste Simon, found that these cells play a crucial role in promoting tumor progression and can be selectively targeted using senolytics.
A team of researchers from Massachusetts General Hospital has identified key molecular step stones in ALD that may provide targets for drug therapy development. The study found that cGAS and Cx32 are promising potential molecular targets for ALD treatment development.
Researchers discovered that hepatitis C virus interacts with the immune system through the interferon-stimulated gene C19orf66, disrupting viral replication machinery and inhibiting its ability to replicate. The study found increased production of C19orf66 in hepatitis C patients, suggesting a potential antiviral effect.
Research reveals TGF-β-driven reduction of cytoglobin (CYGB) in HSCs leads to oxidative DNA damage and liver fibrosis in NASH. CYGB has a protective effect on hepatic parenchymal cells by scavenging hydroxyl radicals.
A new technology has been used to investigate the cellular processes involved in liver fibrosis development, revealing key genes and cell types that correlate with fibrogenesis. The findings have potential applications for diagnostic tools and therapies.
Researchers developed CRISPR-HOT to label specific genes in human organoids, enabling the study of abnormal cell division and cancer development. By disabling the cancer gene TP53, they found that unstructured divisions of abnormal hepatocytes were more frequent, contributing to cancer development.
Researchers developed a CRISPR gene-editing technique that prevented genetic liver disease in mice by introducing a 'minigene' that expresses the enzyme ornithine transcarbamylase. The approach showed promise for treating rare metabolic disorders and other hereditary diseases.
University of California San Diego School of Medicine researchers identify a molecular pathway that allows nonalcoholic steatohepatitis (NASH) to progress into liver cell death. They found that suppressing AMPK and increasing caspase-6 activity can stop progression from fatty liver to NASH and subsequent liver cell death.
Researchers at UC San Diego School of Medicine identified genetic switches that determine whether or not liver cells produce collagen, leading to a potential therapeutic target for liver fibrosis. By manipulating these transcription factors, liver fibrosis progression can be addressed.
Scientists discovered that magnetic nanoparticles can target and treat liver fibrosis by delivering drugs to the affected tissue, reducing inflammation and improving liver function. This new approach offers a potential solution for treating this fatal illness with improved patient outcomes.
The researchers have created a robust cell culture model for the hepatitis E virus, producing approximately 100 times more infectious virus particles than previous models. This allows for extensive studies on the virus and its impact on human liver cells, enabling the identification of key genes involved in the infection.
A new screening method developed by MIT biological engineers can detect DNA damage in cells, which can predict cancer development. The test uses human liver-like cells and has enhanced sensitivity, detecting all nine chemicals tested.
Researchers found that type I interferon disrupts the urea cycle in liver cells, leading to altered serum metabolite concentrations and reduced liver pathology. This regulation affects antiviral immunity and reduces liver damage.
In a mouse model of liver cancer, researchers found that activating the Hippo molecular signaling pathway in tumor cells drives growth, while suppressing it in surrounding healthy cells inhibits tumor growth. Systemic inhibition of Yap and Taz could have unwanted consequences by blocking tumor-suppressing abilities of healthy cells.
Scientists have identified two cellular families involved in liver injury and cancer, with one protein acting as a 'brake' on scar tissue production. The study, published in Nature Communications, sheds new light on the mechanisms behind scarring and its complications in liver disease.
Scientists develop a new method to track lipid metabolism in the body, allowing for clearer distinction between marked and unmarked lipids. This breakthrough enables researchers to examine both normal and pathological deviations in detail, with potential applications for investigating drug side effects on fat metabolism.
Researchers at the University of Edinburgh have identified three new sub-types of cells involved in liver scarring, accelerating the disease progression. The discovery is expected to accelerate the development of new treatments for liver diseases, which affect one in five people in the UK.
Researchers developed a simple, high-throughput protocol to assess the maturation of hepatic-like cells (HPCs) from induced pluripotent stem cells. The protocol enables quick assessment of stem cell differentiation efficacy and helps optimize differentiation conditions for regenerative medicine.
The study reveals a high-definition picture of cell-to-cell signaling in the liver, identifying cellular changes that could drive nonalcoholic steatohepatitis progression. Single-cell analysis also uncovers new information about star-shaped cells and their role in liver fibrosis.
Researchers at the University of Pittsburgh School of Medicine have successfully grown genetically modified miniature human livers in a laboratory setting. These mini livers mimic non-alcoholic fatty liver disease progression and can be used to test therapeutics, providing a valuable tool for understanding and treating diseases.
Researchers at King's College London have identified a new type of cell called hepatobiliary hybrid progenitor (HHyP) that can regenerate liver tissue. HHyPs exhibit stem cell-like properties and may be able to repair liver damage, potentially bypassing the need for transplants.
A comprehensive cell atlas of the human liver reveals previously unknown subtypes of liver cells, including hepatocytes, endothelial cells, and macrophages. The study provides unprecedented resolution into liver cell diversity and how it changes during development or upon disease progression.
Princeton University researchers have developed a scalable cell culture system that allows for detailed investigation of how host cells respond to infection with HBV and HDV. The system, called SACC-PHH, enables chronic HBV infection for up to 40 days, providing unprecedented opportunities to study host responses to hepatitis viruses.
A genetic mutation in the IL18BP gene has been identified as a cause of fatal response to hepatitis A infection. Targeting this pathway may prevent liver failure and death from viral infection.
A human liver cell protein called CXCR4 helps Plasmodium parasites develop into forms capable of infecting red blood cells. Targeting this protein may be a way to block the parasite's life cycle and prevent malaria development.
Researchers found that mouse brain, liver, and pancreas contain populations of young and old cells, with some as old as neurons. This discovery, known as age mosaicism, suggests complex aging processes in organs beyond the brain.
Researchers studied 16 donated livers and found significant impacts of race and gender on hepatocyte yield and viability. The findings suggest expanding liver selection criteria for improved therapeutics development and bioengineering applications.
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 at Princeton University developed a mouse model of hepatitis C by introducing human proteins that allow the virus entry to liver cells. The study found that small mutations in a liver cell protein significantly impact viral replication in mice and humans.
Researchers at UNC and TMIMS discovered that IRF1 protein regulates RARRES3 enzyme, making liver cells hostile to hepatitis A infection. The study provides implications for cellular responses to other RNA viruses like dengue and Zika.
A new study finds that an enzyme involved in liver function also triggers a protective response when liver cells are damaged. By boosting the levels of this enzyme, researchers hope to develop new treatments for acute liver injury.
A review explores how two cell populations respond to organ failure, with one type relying on endoreplication and the other on cell regeneration. This cooperative response allows organs to recover from failure, but also presents tradeoffs that can impact long-term health.
Researchers developed peptide-coated platinum nanoparticles that selectively target and kill liver cancer cells. The nanoparticles are oxidized inside the cell, triggering a cytotoxic effect, while sparing healthy tissue.
Researchers at UNIST have discovered that endotrophin plays a crucial role in producing a pathological microenvironment in liver tissues of chronic liver disease. ETP levels are associated with metabolic dysfunction and systemic insulin resistance, making it a potential diagnostic marker and therapeutic target.
A recent study found that a long-mysterious PCSK9 mutation leads to heart disease by disrupting the interaction between PCSK9 and the LDL receptor. The researchers discovered that a specific sugar chain, heparan sulfate proteoglycan, plays a crucial role in this interaction.
Scientists from Uppsala University have devised a simple method to rescue stressed liver cells by temporarily reducing cellular stress. This approach allows suboptimal human hepatocytes to be revived with restored functionality, increasing the availability of high-quality cells for laboratory experiments.
Researchers at Technical University of Munich discovered that immune cells attacking liver sinusoidal endothelial cells disrupts the organ's blood and nutrient supply, leading to overwhelming damage. A new perforin inhibitor agent has been identified to prevent this lethal process.
Researchers found that yelloweye rockfish have difficulty removing toxic mercury from sensitive liver cells, which can cause damage. The study highlights the potential risks of contaminants on this threatened species, with conservation efforts underway to protect them.
Scientists have created a comprehensive map of individual human liver cells, identifying 20 distinct cell populations and new aspects of the liver's immunobiology. The study, published in Nature Communications, reveals new insights into the liver's cellular landscape and its impact on disease.
A study by Joslin Diabetes Center shows that alanine can activate AMPK, increasing energy production and lowering glucose levels. This finding suggests a new potential way to modify glucose metabolism in the body.
Researchers at ETH Zurich successfully heal genetic disease phenylketonuria in mice using a modified CRISPR/Cas9 system. The technique achieved a high correction rate of up to 60% and restored normal levels of phenylalanine, eliminating the disorder's symptoms.
Researchers at the University of Illinois have discovered how damaged liver cells repair themselves by reprogramming into an early stage of postnatal organ development. The findings reveal that injured liver cells undergo partial reprogramming, which is regulated by a specific RNA-binding protein called ESRP2.
Researchers have successfully created 3D human liver tissue from human stem cells and implanted it into mice with liver disease, demonstrating improved liver function. The study showcases a promising approach to developing human liver tissue implants that could reduce the need for animal testing.
Scientists discover TREM-1 amplifies inflammation, leading to liver scarring and cirrhosis. Targeting this receptor may prevent fibrosis and cancer development.
A study published in Cell found that cells in a three-dimensional environment divide chromosomes correctly, while those in a two-dimensional environment make mistakes. This discovery could help explain why chromosome errors are common in cancerous cells.
Researchers have developed genetically humanized mice that can be persistently infected with Hepatitis Delta Virus (HDV), a common cause of liver fibrosis and cancer. The mice were able to rid themselves of the virus before showing any liver damage, making them an ideal model for testing new treatments.
Scientists at the University of Edinburgh have developed a lab-based system for studying Non-Alcoholic Fatty Liver Disease (NAFLD), the most common cause of liver disease in the developed world. The new tool enables researchers to investigate biological mechanisms and develop effective treatments.
A new study reveals that a malaria parasite manipulates liver cells to survive and reproduce, building strength before invading red blood cells. Disrupting this process by targeting the aquaporin-3 protein may lead to new treatments for malaria before symptoms appear.
Scientists from Cincinnati Children's and UCSF have discovered a mechanism behind an unusual form of tissue regeneration in mice with Alagille syndrome, a rare liver disease. This discovery may lead to a viable treatment for human disease by instructing other types of liver cells to switch identities.
Hemophilia B can be treated for life with a single injection containing disease-free liver cells that produce the missing clotting factor. The finding uses stem-cell strategies and CRISPR/Cas9 gene editing to repair mutations in the patient's FIX gene, allowing normal blood clotting.
Research by BfR scientists reveals that inflammatory processes disrupt liver enzyme function, impairing detoxification capabilities. Fatty liver cells treated with inflammation-promoting substances showed reduced ability to break down foreign substances.
Stanford researchers discover that telomerase-expressing liver cells can rapidly regenerate the liver during normal turnover or tissue damage. These rare cells are evenly distributed throughout the liver's lobules and play a crucial role in enabling the organ to replace damaged cells, potentially leading to cancer.
Researchers discovered that polyploid liver cells can protect the liver against cancer by carrying extra copies of tumor suppressor genes. This finding challenges the notion that polyploidy is a pro-cancer state and suggests it could be an adaptive response within normal liver cells.