Chronic Obstructive Pulmonary Disease (COPD) Research

This study compares the effects of high-tar and low-tar cigarette smoke on COPD airway epithelium using stem cell-derived ALI models, finding stronger responses to high-tar smoke across multiple molecular dimensions.

The paper identifies a cell-selective loss of constitutive redox support in COPD, with reduced PGC-1 target-program output in fibroblasts.

The paper identifies clade B serpins as drivers of basal-to-goblet cell differentiation in COPD, linking them to goblet cell hyperplasia and inflammatory signaling.

This study shows that autonomous MTOR activation in COPD airway epithelial cells impairs lysosome function and contributes to persistent mucus cell metaplasia.

The paper identifies protein interactors of COPD GWAS genes using AP-MS and network analysis, revealing a disease network module involving 8 proteins.

This study evaluates two methods for quantifying lung volume reduction in ex vivo models, showing they can reduce animal testing and improve preclinical assessment of lung treatments.

This study shows that high-fat diet worsens obstructive lung injury by impairing epithelial IGF-1-Akt signaling and promoting epithelial-endothelial interactions.

This study identifies distinct plasma metabolite profiles in COPD patients based on smoking status using GC-MS, finding 23 and 36 altered metabolites in smokers and ex-smokers, respectively, and five diagnostic metabolites with AUC > 0.8.

This study identifies QKI as a regulator of mitochondrial integrity in COPD, showing its protective role against emphysema through maintenance of mitochondrial function.

This study identifies IgG4⁺ plasma cell enrichment and λ-chain-biased BCR remodeling in COPD, linking them to low-grade autoimmunity and chronic inflammation.

This study investigates the role of Piezo1/2 channels in airway smooth muscle cells of COPD patients, finding altered expression and function linked to ECM changes.

This study identifies candidate genes for lung function in Drosophila melanogaster through loss-of-function analysis, finding 11 genes involved in epithelial homeostasis and COPD-related gene expression differences.

This study develops an organ-on-chip model to investigate respiratory-vascular interactions under oxidative stress, revealing how airway injury drives vascular inflammation and remodeling in COPD.

This study shows that loss of Cryptochrome 1 and 2 leads to COPD-like lung disease through disrupted epithelial proliferation and immune homeostasis, and that Nobiletin can alleviate these effects.

This study examines VEGF isoform dynamics in COPD, finding altered VEGF-C and VEGF-A synthesis in fibroblasts and changes in VEGFR3 expression in lung tissue.

This study identifies tissue-resident lymphocytes as drivers of age-associated emphysema by impairing alveolar regeneration and shows IL-7R inhibition can reverse lung damage.

This study shows that Z-AAT expression in AT2 cells causes stress responses and increases emphysema risk in AATD.

This study identifies genetic variants associated with extrapulmonary traits in COPD using genome-wide association analysis across two cohorts.

This study shows that COX4I2 in pericytes drives inflammation and emphysema in COPD by increasing mtROS, and its deletion protects against these effects.

The paper evaluates inconsistencies in reported human airway dimension estimates across studies and introduces an open-access database for standardized geometric inputs.

This study challenges the loss of complexity theory by showing preserved force control in pwCOPD during isometric contractions, suggesting complexity may not be lost in moderate COPD neuromuscular system.

This study shows that Siglec-F protects against elastase-induced lung inflammation and emphysema by regulating airspace macrophages in mice.

This study shows that deleting p16INK4a or targeting p16+ cells reverses alveolar epithelial dysfunction and promotes lung regeneration in emphysema.

This study uses in silico methods to investigate the role of microbial proteins in COPD and explores the therapeutic potential of oleanolic acid.

The paper develops a tunable 3D-alveolosphere model from human primary AEC2 cells to study emphysema, showing key native alveolar features and pathophysiological responses to cigarette smoke extract.

This study shows cigarette smoke induces PPP1R15A through oxidative stress, which reduces pro-inflammatory cytokine production in bronchial epithelial cells.

This study shows that repeated cigarette smoke exposure reduces the proliferation of human lung fibroblasts more than single exposure, with early exposure offering some protection against later exposures.

This study identifies novel therapeutic targets for COPD through meta-analysis of gene expression data and drug repurposing of FDA-approved drugs targeting CXCL9.

This study identifies differentially expressed genes and hub genes in COPD using NGS data and bioinformatics analysis, suggesting potential biomarkers and molecular targets.