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In addition to the liver, stellate cells are present in extrahepatic organs such as the pancreas, lung, kidney, intestine, spleen, adrenal gland, ductus deferens and vocal cords. Hepatic and extrahepatic stellate cells form what has been defined “the stellate cell system”. Besides clear morphological similarities, two main features are peculiar to this type of cells in the liver as well as in other organs: (1) a perivascular location and a distribution typical of a pericyte, particularly when associated with a sinusoidal type of endothelium; and (2) the capability of storing retinoids.1 Although stellate cells, and in particular hepatic stellate cells (HSC), were described more than a century ago, their real physiological and pathophysiological relevance has emerged only in the last 20 years. In these years the knowledge on their profibrogenic role has grown exponentially and the elucidation of the cellular and molecular basis of fibrogenesis has brought important advances in the knowledge of chronic fibrogenic disorders of the liver and pancreas. In this context, understanding the biology of stellate cells, either HSCs or pancreatic stellate cells (PSCs), has been a great adventure for many researchers around the world.
Research on PSCs gradually started in the 1990s following the successful flourish of HSC research. The entrance of PSC into the fibrogenesis research community was highly welcomed, as witnessed by a commentary that I wrote for Gut in 1999.2 Initially, research on PSCs was mainly focused on the demonstration of their potential profibrogenic role and, accordingly, the large majority of …
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