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The wonderful microcosm of the liver: Why is the surface area of the LSEC comparable to that of a tennis court?
In the microscopic world of the liver, liver sinusoidal endothelial cells (LSECs) play a vital role, with a surface area of up to 210 square meters, which is comparable to a tennis court. These special cells are not only unique in structure, but also play a key role in a variety of physiological functions.
Structural features
LSECs are endothelial cells that form the smallest blood vessels in the liver (the sinusoids). Although its volume accounts for only 3% of liver cells, its surface area is astonishing. The cells of LSECs have many openings, called fenestrae, with a diameter of about 100 to 150 nanometers, which occupy about 20% of the surface area of LSECs.
"The remarkable structural features of LSECs make them an efficient material filtration system and an important component of liver metabolism and immune function."
These pores are arranged into so-called "cribriform plates," which help filter the fluid between the sinusoids and the space of Disse and facilitate the traffic of lipoproteins between hepatocytes and the sinusoids. In addition, LSECs also lack an organized basal membrane, which further enhances their filtration function.
Physiological functions
LSECs play a key role in removing harmful substances from the blood. These cells express multiple phagocytic receptors that rapidly internalize waste molecules. Studies have shown that LSECs in rats express multiple types of scavenger receptors, especially the most important one, stabilin 2, which is exclusively present in these cells.
In addition, LSECs express a variety of important receptors, including liver/lymph node-specific ICAM-3-grabbing integrin (L-SIGN) and liver sinusoidal endothelial cell C-type lectin (LSECtin). The body is indispensable in removing harmful substances from the blood."The abundant receptor expression of LSECs confers these cells an important role in innate immunity."
Pathobiology
Liver fibrosis
LSECs also play an important role in the development of liver fibrosis. During the fibrotic process, the porosity of LSECs decreases and an organized basal membrane appears, a phenomenon called tubulization, which often precedes the development of liver fibrosis.
Atherosclerosis
Chylomyelium, produced by intestinal epithelial cells, can be up to 1000 nanometers in diameter and cannot pass through the small pores of LSECs. As chylomicrons gradually become smaller, they can eventually pass through the small pores of LSECs and enter the liver cells for metabolism. Reduced permeability, such as in cirrhosis, diabetes or the elderly, may lead to increased cholesterol levels in the blood and increase the risk of atherosclerosis.
Immune Response
In terms of autoimmune diseases, studies have shown that reduced Fc receptor function in humans leads to increased levels of soluble immune complexes, which are associated with diseases such as systemic lupus erythematosus (SLE) and Sjögren's syndrome. These findings point to a pivotal role for LSECs in the mechanisms of these diseases.
"LSECs not only participate in innate immunity, but also display adaptive immune features, contributing to liver immune tolerance."
Hepatotoxicity
LSECs can sometimes become the primary targets of damage in a condition called small tubule stunting syndrome (SOS). SOS is a pathological state that can lead to hepatocellular hypoxia and liver dysfunction, the main causes of which include the ingestion of certain pathogenic compounds and the use of chemotherapeutic drugs.
Origin and Updates
Normal turnover of LSECs is maintained by LSEC precursor cells in the liver, and bone marrow-derived cells can also replenish the number of LSECs when needed.
As early as the late 19th century and early 20th century, researchers observed that sinus cells in some tissues strongly adsorbed intravenously injected particulate dyes, and gradually came up with the concept of LSECs. Over time, LSECs are thought to collaborate with hepatic macrophages to form a dual-cell model of waste removal.
