1.4 COPD
COPD is the leading cause of respiratory death worldwide, and is also
closely related to heart disease [27]. COPD is characterized by its
persistent symptoms and destruction of lung parenchymal tissue, and
especially during its advanced stages [28]. The cell-specific
mechanisms underlying the pathobiology of COPD are not fully understood.
ScRNA-seq has been used to obtain single-cell resolution and identify
changes in COPD mechanisms, cell phenotypes, and alveolar niche
crosstalk [29, 30]. Maor et al. [30] constructed single-cell RNA
sequencing profiles of explants from subjects with advanced COPD or
control lungs. Those profiles focused on three cell types associated
with COPD pathogenesis: epithelial cells, endothelial cells, and
alveolar macrophages. The profiles identified 33 abnormal types of basal
cells, and identified the CXCL signal transduction that originates from
endothelial cells via a network analysis, and found the common cell type
specific transcriptional aberrations, and revealed that alveolar
macrophages overexpressed metallothionein and HMOX1.
Recently, researchers analysis of 70,030 epithelial cells of lung
adenocarcinoma (LUAD) and normal origin through single-cell RNA
sequencing have identified the alveolar epithelial type II (AT2) cell
subsets that express HHIP, and found that the capillary CXCL motif
chemokine signal is an important cause of COPD alveolar inflammation.
Another conclusion was that the alveolar macrophage subgroup of
metallothionein is enriched in COPD, which provides a more profound
understanding of COPD pathophysiology [31, 32]. At the same time,
scRNA-seq was used to identify cell-specific differences and changes in
individual protein levels that may contribute to the development of
emphysema in severe COPD, More than 20,000 cells were assessed for cell
type markers and cell-specific gene expression characteristics, from
which IGFBP5 and QKI were identified as ciliated epithelial genes
associated with severe COPD [33]. Based on the long-standing
consensus that the immune response primarily mediates the pathology of
chronic obstructive pulmonary disease (COPD), and that exosomes may be
involved in the immune regulation of COPD, Research Scholars sequenced
plasma exosomes and performed single-cell RNA sequencing on peripheral
blood mononuclear cells (PBMCs) from patients with COPD and healthy
controls,they identified 135 mRNAs, 132 lncRNAs, and 359 circRNAs from
exosomes that were differentially expressed in six patients with COPD
compared with four healthy controls, constructed competing endogenous
RNA (ceRNA) and protein–protein interaction (PPI) networks to delineate
the interactions between PBMCs and exosomes within COPD which has
provided a more specific pathological process of COPD by enabling a
series of data analyses of biological information, and constantly
integrating cell types and their interactions.[34]