Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis

The paper identifies shared and opposing genetic risk factors between IPF and hypertension, suggesting potential fibrotic mechanisms and therapeutic considerations.

This study uses single-cell RNA sequencing to identify common and distinct immune aberrations in IPF and FHP, revealing shared monocyte features and disease-specific lymphocyte and receptor repertoires.

This study identifies RPL30 as a hub gene shared in Type 2 Diabetes and Idiopathic Pulmonary Fibrosis through microarray analysis and pathway enrichment.

This study shows that inhibiting SLC1A5, a glutamine transporter, reduces fibrosis by altering fibroblast metabolism and function in a mouse model of lung fibrosis.

This paper identifies six genetic variants significantly associated with idiopathic pulmonary fibrosis susceptibility through meta-analyses and epidemiological evaluation.

This study shows that inhibiting Yap in AT2 stem cells enhances alveolar regeneration and reduces pulmonary fibrosis, while inhibiting Taz worsens fibrosis.

The paper identifies TWIST1 as a critical regulator of myofibroblast activity in IPF using single-nucleus ATAC-seq and scRNA-seq integration.

This study uses patient-derived hydrogels to show IPF fibroblasts exhibit increased inflammation and altered contractility in 3D culture compared to 2D.

This study uses PhIP-Seq to identify novel autoantibodies in ILD patients, revealing a new molecular endotype associated with inflammation and fibrosis.

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 identifies four novel genetic variants associated with IPF survival, including a PCSK6 variant, and suggests PCSK6 as a prognostic biomarker and therapeutic target.

This study identifies TKS5-mediated podosome formation in IPF fibroblasts as a driver of ECM invasion and pulmonary fibrosis, with potential therapeutic targeting via src kinase inhibition.

A stabilized miR-29 mimic, MRG-229, shows efficacy at lower doses and good safety in preclinical models, supporting its development for pulmonary fibrosis.

The paper identifies novel disease-associated genes for idiopathic pulmonary fibrosis using integrative genetic and transcriptomic analyses.

This study performs a large multi-ancestry meta-analysis of IPF genetics, identifying seven novel genome-wide significant loci and highlighting pleiotropy with severe COVID-19 and sex-heterogeneity at the MUC5B locus.

This study uses scRNA-Seq data to identify drug candidates for repurposing in IPF by matching cell transition signatures to drug perturbation signatures.

The paper identifies early fibroblast transitions to a profibrotic state in IPF using scRNA-seq and validates MOXD1 as an early marker.

This study performs a genome-wide meta-analysis across five IPF cohorts, identifying five novel genetic loci associated with idiopathic pulmonary fibrosis.

This study identifies four genetic loci, including one novel, with shared causal variants between severe COVID-19 and idiopathic pulmonary fibrosis (IPF), revealing both shared and distinct biological processes.

The paper shows that inhibiting lactate transporters MCT1 and MCT4 reduces myofibroblast differentiation and pulmonary fibrosis in vitro and in vivo.

This study identifies serum metabolites and biomarkers, including GDF-15, that differentiate idiopathic pulmonary fibrosis from other interstitial lung diseases and healthy controls.

This study shows that CMLD-2 reduces myofibroblast activation and pulmonary fibrosis by inhibiting HuR-mediated osteopontin mRNA stabilization.

This study uses early-stage IPF patient-derived cells to identify proinflammatory and fibrotic states and assess drug responses in airway cells.

This study identifies saracatinib as a potential anti-fibrotic drug effective in multiple models of pulmonary fibrosis, showing equal or superior efficacy compared to existing treatments.

The paper identifies a distal RXFP1 enhancer with reduced activity in fibrotic lung fibroblasts, involving AP-1 transcription factors, and links its activity to JUN and FOS expression.

The paper identifies molecular and structural changes in aging human lungs that contribute to fibrosis and impair lung function.

This paper shows that human bronchial epithelial cell-derived extracellular vesicles reduce pulmonary fibrosis by inhibiting TGF-β-WNT crosstalk through miRNA-mediated mechanisms.

This study shows bortezomib reduces lung fibrosis and fibroblast activation without inhibiting proteasome activity.

This study compares IL11 and IL11RA1 knockout mice, finding IL11 deficiency protects against lung fibro-inflammation but causes infertility, while IL11RA1 deficiency leads to craniosynostosis.