Publications by authors named "Jenny Hetzer"
The role and molecular mechanisms of intermittent fasting (IF) in non-alcoholic steatohepatitis (NASH) and its transition to hepatocellular carcinoma (HCC) are unknown. Here, we identified that an IF 5:2 regimen prevents NASH development as well as ameliorates established NASH and fibrosis without affecting total calorie intake. Furthermore, the IF 5:2 regimen blunted NASH-HCC transition when applied therapeutically.
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- Scientists studied how aging affects inflammation in the intestines of mice by looking at different types of cells.
- They discovered that older intestinal stem cells change in a way that promotes inflammation, and this change can be passed on through cell cultures.
- The researchers also found that a specific signaling pathway (STAT1) plays a key role in how these inflammation-related genes are activated.
Background & Aims: As pancreatic ductal adenocarcinoma (PDAC) continues to be recalcitrant to therapeutic interventions, including poor response to immunotherapy, albeit effective in other solid malignancies, a more nuanced understanding of the immune microenvironment in PDAC is urgently needed. We aimed to unveil a detailed view of the immune micromilieu in PDAC using a spatially resolved multimodal single-cell approach.
Methods: We applied single-cell RNA sequencing, spatial transcriptomics, multiplex immunohistochemistry, and mass cytometry to profile the immune compartment in treatment-naïve PDAC tumors and matched adjacent normal pancreatic tissue, as well as in the systemic circulation.
Article Synopsis
- Chronic liver disease and hepatocellular carcinoma (HCC) pose significant health risks with few effective treatments, largely due to the absence of suitable experimental models for research.
- The study introduces a human liver cell-based model that accurately reflects a clinical prognostic liver signature (PLS), which helps predict the progression of liver disease to HCC.
- By validating the PLS with animal models and patient samples, researchers identify nizatidine, an H2 receptor blocker, as a promising treatment for advanced liver disease and as a preventive measure against HCC, revealing new therapeutic targets through advanced analysis techniques.
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.
View Article and Find Full Text PDFBackground & Aims: Cholangiocyte proliferation and ductular reaction contribute to the onset and progression of liver diseases. Little is known about the role of the transcription factor nuclear factor-κB (NF-κB) in this process. We investigated the activities of the RELB proto-oncogene NF-κB subunit in human cholangiocytes and in mouse models of liver disease characterized by a ductular reaction.
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