Publications by authors named "Marlene Sophia Kohlhepp"
Article Synopsis
- Metabolic dysfunction-associated steatotic liver disease (MASLD) features liver fat accumulation, cell injury, and inflammation, which are explored in this study using a liver-on-a-chip model to simulate disease mechanisms.* -
- The model incorporates mouse liver cells and immune cells to test the effects of acetaminophen and free fatty acids, mimicking acute liver injury and MASLD, respectively.* -
- Results show that while lanifibranor combats inflammation, resmetirom reduces fat buildup in liver cells, highlighting the biochip's utility for testing liver disease treatments.*
Histological techniques based on tissue colorations (e.g., hematoxylin-eosin, Sirius red) and immunostaining remain gold standard methodologies for diagnostic or phenotyping purposes in liver disease research and clinical hepatology.
View Article and Find Full Text PDFChronic liver diseases from varying etiologies generally lead to liver fibrosis and cirrhosis. Among them, non-alcoholic fatty liver disease (NAFLD) affects roughly one-quarter of the world population, thus representing a major and increasing public health burden. Chronic hepatocyte injury, inflammation (non-alcoholic steatohepatitis, NASH) and liver fibrosis are recognized soils for primary liver cancer, particularly hepatocellular carcinoma (HCC), being the third most common cause for cancer-related deaths worldwide.
View Article and Find Full Text PDFBackground And Aims: Nucleotide-binding oligomerization domain-like receptor-family pyrin domain-containing 3 (NLRP3) inflammasome activation has been shown to result in liver fibrosis. Mechanisms and downstream signaling remain incompletely understood. Here, we studied the role of IL-18 in hepatic stellate cells (HSCs), and its impact on liver fibrosis.
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- Monocytes, a type of immune cell, move to areas of injury in the body, and this process is controlled by changes to proteins.
- In people with chronic obstructive pulmonary disease (COPD), a protein called PRMT7 is found in higher amounts in lung tissue, especially in a type of immune cell known as macrophages.
- Reducing PRMT7 can lead to fewer monocytes reaching injury sites, which means less damage and inflammation, suggesting that blocking certain protein changes might help treat inflammatory conditions.
Lymphotoxin β-receptor (LTβR) signalling promotes lymphoid neogenesis and the development of tertiary lymphoid structures, which are associated with severe chronic inflammatory diseases that span several organ systems. How LTβR signalling drives chronic tissue damage particularly in the lung, the mechanism(s) that regulate this process, and whether LTβR blockade might be of therapeutic value have remained unclear. Here we demonstrate increased expression of LTβR ligands in adaptive and innate immune cells, enhanced non-canonical NF-κB signalling, and enriched LTβR target gene expression in lung epithelial cells from patients with smoking-associated chronic obstructive pulmonary disease (COPD) and from mice chronically exposed to cigarette smoke.
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