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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. [8] [6] This state of the stellate cell is the main source of extracellular matrix production in liver injury. [9]
Neuroinflammation is widely regarded as chronic, as opposed to acute, inflammation of the central nervous system. [5] Acute inflammation usually follows injury to the central nervous system immediately, and is characterized by inflammatory molecules, endothelial cell activation, platelet deposition, and tissue edema. [6]
Stellate cells are neurons in the central nervous system, named for their star-like shape formed by dendritic processes radiating from the cell body. These cells play significant roles in various brain functions, including inhibition in the cerebellum and excitation in the cortex, and are involved in synaptic plasticity and neurovascular coupling.
Kupffer cells, also known as stellate macrophages and Kupffer–Browicz cells, are specialized cells localized in the liver within the lumen of the liver sinusoids and are adhesive to their endothelial cells which make up the blood vessel walls. Kupffer cells comprise the largest population of tissue-resident macrophages in the body.
Partial smooth muscle differentiation of a fibroblastic cell; Activation of a stellate cell (e.g. hepatic Ito cells or pancreatic stellate cells). Loss of contractile phenotype (or acquisition of "synthetic phenotype") of a smooth muscle cell. Direct myofibroblastic differentiation of a progenitor cell resident in a stromal tissue.
Inflammatory processes are essential in contributing towards the activation of stellate cells. [2] Therefore, both autocrine and paracrine mediators are involved pancreatic stellate cell activation. [2] Copious amounts of α- SMA-expressing cells are present in fibrotic areas of pancreatic tissue sections in patients with chronic pancreatitis.
Research has shown the pivotal role of the stellate cell, that normally stores vitamin A, in the development of cirrhosis. Damage to the liver tissue from inflammation leads to the activation of stellate cells, which increases fibrosis through the production of myofibroblasts, and obstructs hepatic blood flow. [60]
When these cells have accomplished these tasks, the immune system clears them away. This phenomenon is termed acute senescence. [30] 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. [74]