Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1127258 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29503460_1.fastq.gz | Fastqsanger.gz | |||
| SRR29503460_2.fastq.gz | Fastqsanger.gz | |||
| SRR29503461_1.fastq.gz | Fastqsanger.gz | |||
| SRR29503461_2.fastq.gz | Fastqsanger.gz | |||
| SRR29503462_1.fastq.gz | Fastqsanger.gz |
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Project description:Chronic obstructive pulmonary disease (COPD) is currently the fourth leading cause of morbidity and mortality in the world and is predicted to be the third leading cause of death. It is characterized by chronic airway inflammation, lung destruction and remodeling, resulting in irreversible airflow obstruction. We utilized single cell RNA-sequencing (scRNA-Seq) to identify ferroptotic differences and associated biological processes involved in the pathogenesis of COPD. We performed scRNA-Seq on lung tissue obtained from donors with non-COPD and mild-to-moderate COPD to identify disease-related genes within different cell types. We identified two populations of alveolar macrophages (AMs) in the human lung that were dysregulated in COPD patients. We discovered that M2-like AMs modulate susceptibility to ferroptosis by disrupting lipid and iron homeostasis both in vivo and in vitro. The discrepancy in sensitivity to ferroptosis can be determined and regulated by HO-1. In contrast, M1-like AMs showed the ability to attenuate oxidative stress and exert resistance to ferroptosis. In addition, the expression of genes within M2-like AMs is also involved in defects in phagocytosis and lysosome distortion. Present scRNA-seq transcriptomic analysis provides a rich data source to further explore lung health and disease, and the development of therapeutic strategies specifically targeting ferroptosis-sensitive alveolar macrophages might be used to develop therapeutic targets..
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