详细信息
Mechanisms of Alveolar Type 2 Epithelial Cell Death During Acute Lung Injury ( SCI-EXPANDED收录) 被引量:6
文献类型:期刊文献
英文题名:Mechanisms of Alveolar Type 2 Epithelial Cell Death During Acute Lung Injury
作者:Qi, Xiaofeng[1];Luo, Yali[1,2,3];Xiao, Mengyong[1];Zhang, Qiuju[1];Luo, Jing[1];Ma, Linna[1];Ruan, Linfeng[1];Lian, Nini[1];Liu, Yongqi[1,2,4]
第一作者:Qi, Xiaofeng
通信作者:Luo, YL[1];Liu, YQ[2]
机构:[1]Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent & T, Lanzhou 730000, Gansu, Peoples R China;[2]Gansu Univ Chinese Med, Key Lab Prevent & Treatment Chron Dis Tradit Chine, Lanzhou 730000, Gansu, Peoples R China;[3]Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent & T, Res Combinat Chinese & Western Med Prevent & Treat, Lanzhou 730000, Gansu, Peoples R China;[4]Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent & T, Basic Res Integrat Chinese & Western Med, Lanzhou 730000, Gansu, Peoples R China
第一机构:甘肃中医药大学
通信机构:[1]corresponding author), Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent & T, Res Combinat Chinese & Western Med Prevent & Treat, Lanzhou 730000, Gansu, Peoples R China;[2]corresponding author), Gansu Univ Chinese Med, Prov Level Key Lab Mol Med Major Dis & Prevent & T, Basic Res Integrat Chinese & Western Med, Lanzhou 730000, Gansu, Peoples R China.|[10735]甘肃中医药大学;
年份:2023
卷号:41
期号:12
起止页码:1113
外文期刊名:STEM CELLS
收录:;Scopus(收录号:2-s2.0-85178081866);WOS:【SCI-EXPANDED(收录号:WOS:001077986900001)】;
基金:This article was funded by the National Natural Science Foundation of China (grant no. 82160846), the Key Scientific Research Project of "Double First Class" in Gansu Province(grant no. GSSYLXM-05(017)), the Plan Program of Science and Technology of Lanzhou (grant no. 2022-5-163).
语种:英文
外文关键词:acute lung injury; alveolar type 2 epithelial cell; apoptosis; necrosis; necroptosis; pyroptosis; autophagic cell death; ferroptosis
摘要:Diffuse alveolar epithelial cell (AEC) death occurs extensively during acute lung injury (ALI). Due to the limited proliferative capacity of alveolar type 1 epithelial (AT1) cells, the differentiation and regenerative capacity of alveolar type 2 epithelial (AT2) cells are required to restore the barrier function of AECs. However, during lung injury, AT1 cells are particularly susceptible to injury, and ATII cells die in the presence of severe or certain types of injury. This disruption ultimately results in a hindrance to the ability of AT2 cells to proliferate and differentiate into AT1 cells in time to repair the extensively damaged AECs. Therefore, understanding the mechanism of injury death of AT2 cells may be beneficial to reverse the above situation. This article reviews the main death modes of AT2 cells, including apoptosis, necrosis, necroptosis, pyroptosis, autophagic cell death, and ferroptosis. It compares the various forms of death, showing that various cell injury death modes have unique action mechanisms and partially overlapping pathways. Studying the mechanism of AT2 cell death is helpful in screening and analyzing the target pathway of AEC barrier function recovery. It opens up new ideas and strategies for preventing and treating ALI. Pathogenesis of acute lung injury (ALI) and damage to alveolar type 1 epithelial (AT1) and alveolar type 2 epithelial (AT2) cells. (A) This section describes the major causes of ALI, including severe pulmonary infections (bacterial, viruses, pathogens), pulmonary contusions, inhalation lung injury (drowning, toxic gases), sepsis, disseminated intravascular coagulation (DIC), and severe pancreatitis. (B) The vulnerable part of ALI. As the first barrier for gas exchange between the body and the external environment, the alveolar epithelium has the most significant direct contact area with the external environment. It is the most vulnerable to damage. The alveolar epithelium is mainly composed of AT1 cells and AT2 cells. (C) AT1 cells are prone to massive damage due to stimuli. However, they cannot proliferate and renew themselves. AT2 cells have long been referred to as alveolar progenitor cells of AT1 cells. Once AT1 cells are injured, adjacent AT2 cells are stimulated to proliferation and transdifferentiation into AT1 cells. (D) When faced with severe lung injury, AT2 cells will face the loss of their own proliferation and differentiation ability and even go to death. Currently, the main death modes of AT2 cells include apoptosis, necrosis, necroptosis, pyroptosis, autophagic cell death, and ferroptosis.
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