In normal liver, stellate cells are described as being in a
quiescent state. Quiescent stellate cells represent 5-8% of the total number of liver cells. Each cell has several long cytoplasmic protrusions that extend from the cell body and wrap around the sinusoids. The
lipid droplets in the cell body store
vitamin A as
retinyl palmitate. Hepatic stellate cells store 50–80% of the body's vitamin A. When the liver is damaged, stellate cells can change into an
activated state. The activated stellate cell is characterized by proliferation, contractility, and
chemotaxis. This change is seen as a
transdifferentiation whereby the cells lose their stellate shape and acquire that of
myofibroblasts. This attribute makes it a key factor in the pathophysiology of the liver. The amount of stored vitamin A decreases progressively in liver injury. Studies have also shown that in vivo activation of hepatic stellate cells by agents causing liver fibrosis can eventually lead to
senescence in these cells, marked by increased SA-beta-galactosidase staining, as well as
p53 accumulation and activation of
Rb—hallmarks of
cellular senescence. Senescent hepatic stellate cells have been demonstrated to limit liver fibrosis by activating interactions with
NK cells. Senescence of hepatic stellate cells could prevent progression of liver fibrosis, although this has not been implemented as a therapy, and would carry the risk of hepatic dysfunction. ==History==