Experimental Insights into MASLD and MASH
Nov
12
2023
Ballroom A
-
Hynes Convention Center
4:30
- 6:00 PM EST
Speakers
Description
This scientific session focuses on novel experimental approaches and molecular insights into the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD), exploring potential therapeutic targets for its treatment.
Abstracts
- ROLE OF AUTOPHAGY IN HEPATIC ACETYLOME REGULATION
- LIPID INDUCED ENDOTHELIAL INTERCELLULAR ADHESION MOLECULE 1 (ICAM1) PROMOTES METABOLIC DYSFUNCTION-ASSOCIATED STEATOHEPATITIS
- HEPATOCYTE-SPECIFIC HIF-1α DELETION ACCELERATES NON-ALCOHOLIC STEATOHEPATITIS PROGRESSION TO LIVER FIBROSIS
- GENETIC ABLATION OF CD4 T CELLS IN MICE ATTENUATES LIVER INJURY, INFLAMMATION, AND FIBROSIS IN NONALCOHOLIC STEATOHEPATITIS
- SINGLE-CELL ANALYSES IDENTIFY ENRICHMENT OF Th1 CELLS IN MURINE NONALCOHOLIC STEATOHEPATITIS
- INTESTINE SPECIFIC HIF-1α OVEREXPRESSION AMELIORATES WESTERN DIET-INDUCED MASLD AND METABOLIC PHENOTYPES
Objectives
- Understand the diverse molecular pathways and cellular mechanisms involved in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD), including the roles of endothelial cell adhesion molecules, autophagy, and immune cell function.
- Assess the significance of HIF-1α expression in both hepatocytes and intestinal cells, and its dual role in promoting or attenuating metabolic dysfunction-associated steatotic liver disease (MASLD).
- Analyze potential therapeutic targets for MASLD treatment, exploring the feasibility of targeting molecules involved in hepatic steatosis, inflammation, and fibrosis, and evaluate their potential clinical implications.