Basal-like Progenitor Cells: A Review of Dysplastic Alveolar Regeneration and Remodeling in Lung Repair.
Basal-like Progenitor Cells: A Review of Dysplastic Alveolar Regeneration and Remodeling in Lung Repair.
复制标题
基底样祖细胞：对肺修复中肺泡再生和重塑的综述。
DOI：
10.1016/j.stemcr.2020.09.006
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发表时间：
2020-11-10
影响因子：
5.9
通讯作者：
Vaughan AE
中科院分区：
文献类型：
--
作者：
Fernanda de Mello Costa M;Weiner AI;Vaughan AE
尽管呼吸系统至关重要，但严重损伤后肺修复的确切机制仍不清楚。肺泡2型细胞(AT2)可以自我更新并分化为1型肺泡型细胞(AT1)的概念并不完全包括这些祖细胞受到疾病严重影响的情况，例如H1N1流感或SARS-CoV-2(新冠肺炎)。肺内p63+祖细胞在小鼠中是一种罕见的细胞类型，但在人类中可能包含更多的经典基底细胞，在如此严重的损伤环境中被激活，增殖并迁移到受损的肺泡实质中，提供短期的“紧急”益处。虽然这些细胞的命运存在争议，但大多数研究表明，它们代表着一种适应不良的修复途径，对呼吸道细胞类型有命运限制，很少分化为AT2或AT1细胞。在这里，我们讨论了肺内基底样p63+细胞在肺泡再生中的作用，并建议一个统一的模型来指导未来的研究。在这篇评论文章中，Costa等人。讨论肺内“基底样”p63+祖细胞在严重肺损伤，尤其是由呼吸道病毒引起的肺损伤后再生/重塑中的作用。这种修复机制有助于上皮屏障功能的恢复，但最终会在肺泡实质中产生不同类型的细支气管细胞，从而代表一种发育异常、适应不良的上皮细胞对损伤的反应。
Despite the central importance of the respiratory system, the exact mechanisms governing lung repair after severe injury remain unclear. The notion that alveolar type 2 cells (AT2s) self-renew and differentiate into alveolar type 1 cells (AT1s) does not fully encompass scenarios where these progenitors are severely affected by disease, e.g., H1N1 influenza or SARS-CoV-2 (COVID-19). Intrapulmonary p63+ progenitor cells, a rare cell type in mice but potentially encompassing more numerous classic basal cells in humans, are activated in such severe injury settings, proliferating and migrating into the injured alveolar parenchyma, providing a short-term “emergency” benefit. While the fate of these cells is controversial, most studies indicate that they represent a maladaptive repair pathway with a fate restriction toward airway cell types, rarely differentiating into AT2 or AT1 cells. Here, we discuss the role of intrapulmonary basal-like p63+ cells in alveolar regeneration and suggest a unified model to guide future studies. In this review article, Costa et al. discuss the role of “basal-like” intrapulmonary p63+ progenitor cells in regeneration/remodeling after severe lung injury, especially that caused by respiratory viruses. This repair mechanism serves to aid in restoration of epithelial barrier function but ultimately generates bronchiolar cell types in the alveolar parenchyma, thus representing a dysplastic, maladaptive epithelial response to injury.
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影响因子：
64.5
作者：
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Jay P
DOI：
10.1073/pnas.1522376113
发表时间：
2016-04-05
影响因子：
11.1
作者：
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通讯作者：
Heaton, Nicholas S.
DOI：
10.4049/jimmunol.1800671
发表时间：
2018-10-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Keeler SP;Agapov EV;Hinojosa ME;Letvin AN;Wu K;Holtzman MJ
通讯作者：
Holtzman MJ