Hepatic stellate cell hyperplasia

The phenomenon that the number of hepatic stellate cells increases through division and reproduction is called hepatic stellate cell proliferation, which is a very important key link in the pathogenesis and development of liver fibrosis. Hepatic stellate cells (HSCs) have various names, such as liver fat-storing cells (FSCs), lipid cells (1ipocytes), vitamin A-storingcells, pericytes (perisinusoidalcell), Ito cells, etc. It is the main source of ECM. HSC activates and transforms into myofibroblast-like cells (MFC). HSC is the ultimate target cell for various fibrogenic factors. Under normal circumstances, hepatic stellate cells are at rest. When the liver is damaged by inflammation or mechanical stimulation, hepatic stellate cells are activated, and their phenotype changes from resting to activated. Activated hepatic stellate cells, on the one hand, participate in the formation of liver fibrosis and the reconstruction of intrahepatic structures through proliferation and secretion of extracellular matrix, and on the other hand, increase the intrahepatic sinusoidal pressure through cell contraction. There are two types of hepatic stellate cell proliferation: physiological and pathological. Occurs because of adaptation to physiological needs, and the extent of which does not exceed the normal limit is called physiological hyperplasia. After some tissues of the human body are damaged, the compensatory hyperplasia of the rest is also physiological hyperplasia. Hyperplasia caused by pathological causes beyond the normal range is called pathological hyperplasia. Physiological hyperplasia is divided into compensatory hyperplasia and endocrine hyperplasia. The mechanism of physiological proliferation is not fully understood at present. Pathological hyperplasia is mostly related to hormonal stimulation; tumorous hyperplasia caused by tumor cell proliferation also belongs to the scope of pathological hyperplasia. But conventionally, hyperplasia refers to benign non-tumorous lesions. Although hyperplasia and hypertrophy are two different concepts, in fact hypertrophy often occurs at the same time. Compensatory hyperplasia that occurs due to adaptation to physiological needs or after injury can enhance or compensate for local metabolic and functional changes, which is beneficial to the body. But pathological hyperplasia is often harmful to the body. Benign prostatic hyperplasia (BPH) is the most common disease in older men and the most common benign tumor in men. BPH is often associated with a series of irritation and lower urinary tract symptoms (LUTS), which negatively affects the quality of life of patients. Untreated BPH can cause some complications, the most common of which are acute urinary retention (AUR), gross hematuria, recurrent urinary tract infections, symptoms of urinary tract obstruction, bladder stones, and relatively rare renal failure. HSC is located in the Disse space, next to sinusoidal endothelial cells (SEC) and hepatocytes. Its morphology is irregular, the cell body is round or irregular, and several stellate cell processes often extend around the hepatic sinus. In addition, HSC also extended the cell process to make contact with hepatocytes and adjacent stellate cells. The cytoplasm of HSC contains 1 to 14 lipid droplets rich in vitamin A and triglycerides with a diameter of about 1.0 to 2.0 μm. The cytoplasm is rich in free ribosomes, rough endoplasmic reticulum, and a developed Golgi complex. The nucleus is irregular in shape. Due to the squeeze of lipid droplets, the nucleus often has one or more depressions, and one or two nucleoli can be seen in the nucleus. The number of HSCs in normal liver is very small, accounting for only 5% to 8% of the total number of hepatocytes and 1.4% of the total volume. However, the three-dimensional distribution and extension of HSC are sufficient to cover the entire hepatic sinusoidal microcirculation.

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