Pulmonary endogenous progenitor stem cell subpopulation: Physiology, pathogenesis, and progress

Liu, Di; Xu, Chang; Jiang, Lai; Zhu, Xiaoyan

doi:10.1016/j.jointm.2022.08.005

Cited by 2 publications

(1 citation statement)

References 214 publications

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“…In the last decades, studies have been conducted to elucidate the populations of lung epithelial cells that modulate lung injury and repair, as well as the underlying mechanisms of such responses. To date, AECII stand out as they have been extensively investigated and are proposed as the progenitors of the adult lung alveolus [62]. AECII play a pivotal role in surfactant synthesis, secretion, and recycling.…”

Section: Discussionmentioning

confidence: 99%

Glycogen Synthase Kinase-3 Inhibition by CHIR99021 Promotes Alveolar Epithelial Cell Proliferation and Lung Regeneration in the Lipopolysaccharide-Induced Acute Lung Injury Mouse Model

Fernandes,

Barbosa-Matos,

Borges-Pereira

et al. 2024

IJMS

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Acute respiratory distress syndrome (ARDS) is a life-threatening lung injury that currently lacks effective clinical treatments. Evidence highlights the potential role of glycogen synthase kinase-3 (GSK-3) inhibition in mitigating severe inflammation. The inhibition of GSK-3α/β by CHIR99021 promoted fetal lung progenitor proliferation and maturation of alveolar epithelial cells (AECs). The precise impact of CHIR99021 in lung repair and regeneration during acute lung injury (ALI) remains unexplored. This study intends to elucidate the influence of CHIR99021 on AEC behaviour during the peak of the inflammatory phase of ALI and, after its attenuation, during the repair and regeneration stage. Furthermore, a long-term evaluation was conducted post CHIR99021 treatment at a late phase of the disease. Our results disclosed the role of GSK-3α/β inhibition in promoting AECI and AECII proliferation. Later administration of CHIR99021 during ALI progression contributed to the transdifferentiation of AECII into AECI and an AECI/AECII increase, suggesting its contribution to the renewal of the alveolar epithelial population and lung regeneration. This effect was confirmed to be maintained histologically in the long term. These findings underscore the potential of targeted therapies that modulate GSK-3α/β inhibition, offering innovative approaches for managing acute lung diseases, mostly in later stages where no treatment is available.

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Section: Discussionmentioning

confidence: 99%