Publications by authors named "S E Pors"
Characterization of six clinical drugs and dietary intervention in the nonobese CDAA-HFD mouse model of MASH and progressive fibrosis.
Am J Physiol Gastrointest Liver Physiol
January 2025
Article Synopsis
- The CDAA-HFD mouse model is utilized to study metabolic dysfunction-associated steatohepatitis (MASH) by simulating disease progression and testing various treatments.
- The study evaluated several drugs, including semaglutide and lanifibranor, for their effectiveness in reversing fibrosis and improving liver conditions after different time points on the CDAA-HFD diet.
- Findings indicate that while semaglutide and lanifibranor showed partial benefits when used preventively, elafibranor was the only drug that improved fibrosis significantly, highlighting the importance of timing in pharmacological interventions.
This study comprehensively validated the bleomycin (BLEO) induced mouse model of IPF for utility in preclinical drug discovery. To this end, the model was rigorously evaluated for reproducible phenotype and TGFβ-directed treatment outcomes. Lung disease was profiled longitudinally in male C57BL6/JRJ mice receiving a single intratracheal instillation of BLEO (n = 10-12 per group).
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- The study investigates whether human platelet lysate (hPL) and umbilical cord plasma can improve vascularization and survival of human ovarian tissue transplanted into immunodeficient mice.
- The design involved transplanting ovarian tissue into nude mice and administering PRP or saline while assessing vascularization and gene expression related to angiogenesis and apoptosis over time.
- Results showed increased vascularization over time but no significant differences between hPL and the control; gene expression indicated changes in apoptosis markers, and ultrasound monitoring proved useful but did not show enhanced follicular survival.
Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease, encompasses steatosis and metabolic dysfunction-associated steatohepatitis (MASH), leading to cirrhosis and hepatocellular carcinoma. Preclinical MASLD research is mainly performed in rodents; however, the model that best recapitulates human disease is yet to be defined. We conducted a wide-ranging retrospective review (metabolic phenotype, liver histopathology, transcriptome benchmarked against humans) of murine models (mostly male) and ranked them using an unbiased MASLD 'human proximity score' to define their metabolic relevance and ability to induce MASH-fibrosis.
View Article and Find Full Text PDFNon-alcoholic steatohepatitis (NASH) is emerging as a major cause of hepatocellular carcinoma (HCC), however, it is not resolved if compounds in late-stage clinical development for NASH may have additional therapeutic benefits in NASH-driven HCC (NASH-HCC). Here, we profiled monotherapy with semaglutide (glucagon-like-receptor-1 receptor agonist) and lanifibranor (pan-peroxisome proliferator-activated receptor agonist) in a diet-induced obese (DIO) mouse model of NASH-HCC. Disease progression was characterized in male C57BL/6 J mice fed the GAN (Gubra Amylin NASH) diet high in fat, fructose and cholesterol for 12-72 weeks (n = 15 per group).
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