A hepatocyte is a cell of the main parenchymal tissue of the liver. Hepatocytes make up 55-65% of the liver's mass. Hepatocyte damage plays an important role in the process of liver disease. In this article, we focus on hepatocellular injury and its relationship with liver disease.
The liver is made up of hepatocytes, which are extremely small and invisible to the naked eye. They must be seen through a microscope. Human liver has about 2.5 billion hepatocytes, and 5000 hepatocytes make up a hepatic lobule, so the total number of hepatic lobules in human liver is about 500,000. Hepatocytes are polygonal, with a diameter of about 20-30 (micrometers) and 6-8 faces. The size varies under different physiological conditions, For example, the liver cells become large when starved. The surface of each hepatocyte is divided into three types: sinusoidal surface, hepatocyte surface, and bile duct surface.
Regardless of the cause of liver disease, hepatocellular damage is a common pathology. Hepatocytes are susceptible to toxic substances such as drugs and alcohol, lipotoxicity, hepatitis virus, autoimmunity, metabolic abnormalities, and ischemic hypoxia. There are three ways of liver cell damage as follows:
The normal structure and function of the cell membrane is an important guarantee for the cell to perform physiological functions. Abnormal fluidity of the biofilm causes cell function disorders. In the liver, the lipids of hepatocyte and mitochondrial membrane are rich in polyunsaturated fatty acids. And polyunsaturated fatty acids are not only more easily oxidized than saturated fatty acids, but also easier to synthesize phospholipids and triglycerides. Moreover, hepatocyte mitochondrial metabolism is active. These factors make liver cell membranes more susceptible to free radical and lipid peroxidation damage.
Mitochondrial damage is also an important component of liver cell damage. A fatty liver model of rats on a high-fat diet showed that the mitochondria of the liver cells increased, swelled, and the crusts fell off and decreased. In some cases, high-density crystal-like substances were deposited, and the content of ATP decreased in liver. Therefore, patients with steatohepatitis may have mitochondrial structural damage and reduced ATP reserves.
The physiological role of the endoplasmic reticulum (ER) is to modify, fold and oligomerize about 1/3 of the proteins synthesized in the cell to form the correct conformation, and participate in lipid metabolism and steroid hormone synthesis and calcium storage. Hepatitis virus infection leads to cell water loss, dehydration, and ribosome shedding on the rough endoplasmic reticulum, and then leads to the loss of the starting site for protein synthesis. Bacterial infection and invasion of toxic substances affect the detoxification function of liver cells and the endoplasmic reticulum becomes hypertrophy.
Hepatocellular Injury is closely related to the progression of liver disease. As liver damage worsens, liver disease can progress from hepatitis to cirrhosis and eventually develop into liver cancer.
Figure 1. The Progress of Hepatocellular Injury
After hepatocyte membrane damage, membrane fluidity decreases and membrane permeability increases. Decreased fluidity of the hepatocyte membrane results in impaired membrane-related enzyme activity, receptors, and transport functions, inhibiting hepatocyte function. Hepatocyte injury and death (especially hepatocyte necrosis) activates immune cells such as stellate cells, Kupffer cells, natural killer cells and promote liver inflammation.
In the case of chronic liver disease, Hepatocyte injury and death leads to altered collagen metabolism, promote the formation of fibrosis and cirrhosis. Therefore, liver cell damage is closely related to the progress of clinical common liver diseases. Treatment strategies that promote hepatocyte repair have a positive impact on the treatment of liver disease.
Additionally, for the treatment of liver cell injury, a comprehensive treatment strategy should be adopted to control the etiology, block the injury and continue to aggravate, and promote liver cell regeneration and repair. This not only helps to maintain the number, structure and function of liver parenchymal cells, but also helps to delay the progress of fibrosis and prevent the occurrence of cirrhosis and hepatocellular carcinoma.
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