期刊
ANNUAL REVIEW OF PATHOLOGY-MECHANISMS OF DISEASE
卷 17, 期 -, 页码 515-546出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-pathol-042320-030240
关键词
cellular senescence; interstitial lung disease; pulmonary fibrosis; single-cell RNA sequencing
类别
The pathogenesis of idiopathic pulmonary fibrosis (IPF) involves a complex interplay of various cell types and signaling pathways. Novel bioinformatics tools can help discover disease pathways, cell-specific mechanisms, and cell-cell interactions.
The pathogenesis of idiopathic pulmonary fibrosis (IPF) involves a complex interplay of cell types and signaling pathways. Recurrent alveolar epithelial cell (AEC) injury may occur in the context of predisposing factors (e.g., genetic, environmental, epigenetic, immunologic, and gerontologic), leading to metabolic dysfunction, senescence, aberrant epithelial cell activation, and dysregulated epithelial repair. The dysregulated epithelial cell interacts with mesenchymal, immune, and endothelial cells via multiple signaling mechanisms to trigger fibroblast and myofibroblast activation. Recent single-cell RNA sequencing studies of IPF lungs support the epithelial injury model. These studies have uncovered a novel type of AEC with characteristics of an aberrant basal cell, which may disrupt normal epithelial repair and propagate a profibrotic phenotype. Here, we review the pathogenesis of IPF in the context of novel bioinformatics tools as strategies to discover pathways of disease, cell-specific mechanisms, and cell-cell interactions that propagate the profibrotic niche.
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