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Alveolar type 2 (AT2) cells, or type II pneumocytes, are specialized epithelial cells that play a vital role in maintaining lung homeostasis and responding to injury [StatPearls: NBK557541]. Although they cover only a small fraction of the alveolar surface, they are responsible for the production, secretion, and recycling of pulmonary surfactant, which is essential for reducing surface tension and preventing alveolar collapse [PMID: 16759237]. Furthermore, AT2 cells act as the resident progenitor cells of the alveolar epithelium; they possess the capacity for self-renewal and can differentiate into alveolar type 1 (AT1) cells to repair the gas-exchange surface after damage [PMID: 23778143]. In clinical medicine, AT2 cell dysfunction is central to the pathology of idiopathic pulmonary fibrosis (IPF) and neonatal respiratory distress syndrome, and these cells are the primary targets for SARS-CoV-2 infection in the lower respiratory tract [PMID: 32142651]. While AT2 cells are not a single molecular target, they are the focus of surfactant replacement therapies and regenerative medicine approaches aimed at stimulating endogenous repair mechanisms [PMID: 24169011].
Exogenous surfactant replacement therapy compensates for AT2 cell deficiency or dysfunction [StatPearls: NBK544271]. Growth factors like Palifermin (KGF) target the FGFR2b receptor on AT2 cells to promote proliferation, survival, and alveolar repair [PMID: 24169011].
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