Abstract
Vitamin A-storing cells in the liver (also called as hepatic stellate cells, lipocytes, interstitial cells, fat-storing cells, or Ito cells) exist in the space between parenchymal cells and liver sinusoidal endothelial cells of the hepatic lobule, and store 50-80% of vitamin A in the whole body as retinyl palmitate in lipid droplets in the cytoplasm. In physiological conditions, these cells play pivotal roles in the regulation of vitamin A homeostasis. In pathological conditions such as hepatic fibrosis or liver cirrhosis, hepatic stellate cells lose vitamin A, and synthesize a large amount of extracellular matrix (ECM) components including collagen, proteoglycan, glycosaminoglycan, and adhesive glycoproteins. Morphology of these cells also changes from the star-shaped stellate cells to that of fibroblasts or myofibroblasts. The hepatic stellate cells are now considered to be targets of hepatic fibrosis or liver cirrhosis. Hepatic stellate cells are activated by adhering to the parenchymal cells and lose stored vitamin A during hepatic regeneration. Vitamin A-storing cells exist in extrahepatic organs such as pancreas, lung, kidney, and intestine. Vitamin A-storing cells in the liver and extrahepatic organs form a cellular system. The research of the vitamin A-storing cells has developed and expanded vigorously, and tremendous number of reports have been published during these two decades. The frontiers of the research will be summarized and discussed in this review.
