The understanding of mechanism during conversion from sepsis to sepsis-related ARDS remains limited. In this study, we collected gene expression matrix from the Gene Expression Omnibus (GEO) database and constructed networks using weighted gene co-expression network analysis (WGCNA) to identify the consensus and opposite modules between sepsis and sepsis-induced ARDS and obtained 27 consensus modules associated with sepsis and sepsis-related ARDS, including one model (160 genes) with opposite correlation and 1 sepsis-ARDS specific model with 34 genes. Differentially expressed genes analysis, functional enrichment and protein-protein interactions analyses of candidate genes were performed; 15 of these genes showed different expressions in sepsis-induced ARDS patients, compared with sepsis patients; genes were enriched in processes associated with ribosome, tissue mechanics and extracellular matrix. Feature selection analysis revealed that three genes, , and , showed moderate performance in identifying sepsis-induced ARDS from sepsis. Ribosome-related genes indicate crucial roles in the development of sepsis-induced ARDS.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806251PMC
http://dx.doi.org/10.1080/21655979.2021.1909961DOI Listing

Publication Analysis

Top Keywords

sepsis-induced ards
16
genes
9
weighted gene
8
gene co-expression
8
co-expression network
8
network analysis
8
analysis wgcna
8
sepsis sepsis-related
8
sepsis-related ards
8
gene expression
8

Similar Publications

Pulmonary endothelial cell (EC) activation is a key factor in acute respiratory distress syndrome (ARDS). In sepsis, increased glycolysis leads to lactate buildup, which induces lysine lactylation (Kla) on histones and other proteins. However, the role of protein lactylation in EC dysfunction during sepsis-induced ARDS remains unclear.

View Article and Find Full Text PDF

Background: Sepsis is a systemic inflammatory response caused by infection. When this inflammatory response spreads to the lungs, it can lead to acute lung injury (ALI) or more severe acute respiratory distress syndrome (ARDS). Pulmonary fibrosis is a potential complication of these conditions, and the early occurrence of pulmonary fibrosis is associated with a higher mortality rate.

View Article and Find Full Text PDF

Background: Acute respiratory distress syndrome (ARDS) is a life-threatening and heterogeneous disorder leading to lung injury. To date, effective therapies for ARDS remain limited. Sepsis is a frequent inducer of ARDS.

View Article and Find Full Text PDF

Introduction: Sepsis-induced acute lung injury (ALI), a critical sequela of systemic inflammation, often progresses to acute respiratory distress syndrome, conferring high mortality. Although UMI-77 has demonstrated efficacy in mitigating lung injury in sepsis, the molecular mechanisms underlying its action have not yet been fully elucidated.

Methods: This study aimed to delineate the mechanism by which UMI-77 counteracts sepsis-induced ALI using comprehensive transcriptomic and metabolomic analyses.

View Article and Find Full Text PDF

Acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS), result from pulmonary edema and alveolar-capillary barrier disruption due to inflammation, often triggered by conditions like sepsis. Sepsis-induced ALI (SALI) involves extensive damage to vascular endothelium and alveolar epithelium, leading to respiratory failure. Our study explores ferroptosis, an iron-dependent cell death pathway, and calcium dysregulation in SALI.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!