Liver fibrosis is an important pathological basis for the progression of a variety of chronic liver diseases to cirrhosis and liver cancer. The occurrence, development and prognosis of liver fibrosis are regulated by a variety of cytokines, chemokines, molecular models of injury (DAPs) and signaling pathways. Recent studies have found that apoptosis, autophagy, pyroptosis, ferroptosis, and cuproptosis are closely related to the progression of liver fibrosis, and the process of liver fibrosis can be delayed or even reversed by regulating or inhibiting the death of these cells. Yu's group recently published a paper in Cell Death Discovery (if=7.).0 q2) (if=7.).0 q2), which was reviewed, hoping to have some reference significance for the prevention and treatment of liver fibrosis.
Programmed cell death (programmed death) is an important regulatory mechanism for the occurrence, progression and reversal of liver fibrosis, and has become a new target for the development of antifibrotic drugs. Small molecule drugs that target this can delay or reverse the progression of liver fibrosis. However, different types of cells have programmed death and have different mechanisms of action. There is a large amount of apoptosis and ferroptosis in hepatocytes, and when they appear in hepatic stellate cells, they are inhibited. In stark contrast, autophagy is present in hepatocytes, which inhibits inflammation and reduces liver fibrosis; In hepatic stellate cells (HSCs), autophagy promotes lipid autophagy and fibrosis. Targeting HSCs, inducing apoptosis and ferroptosis, or blocking autophagy, can reverse liver fibrosis. However, how to target HSCs without damaging normal hepatocytes is a major problem. This study will provide new ideas for the clinical prevention and treatment of liver fibrosis.
This illustration was created by the Gethorp cartographic team
Lu Julu, a graduate student of Jiangsu Institute of Schistosomiasis Control, researcher Yu Chuanxin, and associate researcher Song Lijun served as the corresponding authors of **.
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