Abstract

Hepatic stellate cells (HSCs) are located in the space of Disse, between sinusoidal epithelial cells and hepatocytes. When the liver is injured chronically by alcohol, toxins, viruses, or nonalcoholic steatohepatitis, HSCs are activated. Activated HSCs are transdifferentiated into proliferative myofibroblasts which secrete extracellular matrix and exhibit contractile properties. HSCs may be an effective target to treat liver fibrosis. HSCs can communicate with neighboring cells such as hepatocytes, sinusoidal endothelial cells, Kupffer cells, and immune cells that regulate the activation of HSCs. The secretion of cytokines has led to HSC activation by the cell types mentioned, adipocytes are also known to release cytokines. The role of adipocytes in HSC activation has been rarely reported. This research aims to explore the roles of adipocyte-hepatic stellate cell crosstalk in liver fibrosis. At this annual meeting preliminary gene expression of activation markers, α-smooth muscle actin and type I collagen fiber, in HSCs will be discussed. Institutional Development Award (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under grant #P20GM103424-21. Grambling State University Title 3 Program (Award #P01B220013). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

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