Wim Timens

The paper identifies a novel asthma-associated epithelial differentiation trajectory involving KRT14+ basal cells and hillock-like cells that contributes to airway inflammation and remodelling in childhood-onset asthma.

This study shows E-cigarette vapour induces cellular senescence in primary human lung fibroblasts, impairing tissue repair, but not in a mouse model.

This study shows that SASP from senescent fibroblasts in severe early-onset COPD promotes paracrine senescence, inflammation, and ECM dysregulation in surrounding fibroblasts.

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 shows RANKL promotes alveolar epithelial cell expansion in mice and humans, suggesting RANKL/RANK signaling as a conserved pathway for lung tissue repair.

This study investigates the relationship between SERPINA3, osteoprotegerin (OPG), and mast cell mediators in bronchiolitis obliterans syndrome (BOS) and finds they are expressed by mast cells and may form a complex contributing to airway remodeling.

The paper identifies fibroblast-derived osteoglycin as a key factor promoting epithelial cell repair and presents its active fragment as a potential therapeutic for lung diseases.

This study examines compositional changes in the lung extracellular matrix across stages of acute respiratory distress syndrome (ARDS) and duration, revealing shifts in collagen and other matrix proteins.

The paper identifies twelve novel genetic risk loci for lung cancer subtypes through multi-ancestry GWAS and shows smoking-independent genetic risk.

The paper identifies shared genetic variants between critically ill COVID-19 and idiopathic pulmonary fibrosis by integrating GWAS with context-specific eQTLs and transcriptomics.

The paper compares ECM protein expression in severe-early onset and moderate COPD to controls, identifying ECM signatures linked to disease severity and subtypes.

This study investigates RANKL's role in lung epithelial cell regeneration, finding it promotes type II alveolar epithelial cell regeneration and may contribute to lung tissue repair.

This study shows that 3D fibrotic ECM hydrogels alter fibroblast fiber organization and mechanical properties, promoting pro-fibrotic responses.

This study identifies ECM gene and protein changes in COPD lung tissue linked to cellular senescence, confirming in vivo associations previously observed in vitro.

RNA sequencing in bronchial biopsies from wheezing infants and children < 2 years shows evidence for an airway epithelial hillock-to-squamous differentiation pathway that marks the development of asthma.

This study identifies seven age-associated ECM proteins with increased expression in human lung tissue and demonstrates age-related differences in specific lung compartments.

The paper uses multi-omics approaches to identify genes and plasma proteins associated with COVID-19, finding ABO plasma protein as a causal risk factor.

The paper identifies co-expressed genes with ACE2 and TMPRSS2 in lung tissue and finds many have drug interactions, suggesting potential targets for COVID-19 therapeutics.

This study uses Mendelian randomization to examine if ACE inhibitors or cardiometabolic risk factors affect lung ACE2 and TMPRSS2 expression or plasma ACE2 levels, finding no overall association.

The paper identifies a corticosteroid-sensitive gene cluster in COPD patients using asthma-derived transcriptomic signatures and links it to mast cell numbers and lung function improvement.

This study uses single-cell RNA sequencing to analyze smoking effects on bronchial epithelial cell types, identifying molecular changes and a novel subpopulation linked to premalignant lesions.

This study identifies three new genetic loci associated with idiopathic pulmonary fibrosis and confirms 11 previously reported ones, highlighting mTOR signaling and mitotic spindle-assembly genes in disease susceptibility.

The paper identifies 12 novel COPD loci and candidate causal genes using GWAS and lung eQTL data from 129 risk loci.