Paul J. Wolters

This study compares molecular features of SSc-NSIP and SSc-UIP with IPF, finding shared epithelial changes and distinct fibroblast programs.

This study identifies DLGAP5 as a driver of pulmonary vascular remodeling in PAH by promoting cell proliferation and survival through cyclin A2 and DEPDC1 upregulation and BIM suppression.

This study identifies age-related epigenetic changes in AT2 cells that promote basal cell metaplasia, contributing to idiopathic pulmonary fibrosis.

The paper compares collagen organization and crosslinking in IPF and NR-ARDS, finding differences in collagen maturity despite similar collagen content.

This study investigates how pirfenidone and nintedanib affect the growth and differentiation of human alveolar type 2 cells in organoid cultures, revealing differences in their impact on surfactant protein C expression and cell identity.

The paper identifies an early profibrotic alveolar type 2 cell signature in lung fibrosis using single-cell RNA sequencing and shows that p53 inhibition can reverse fibrosis.

The paper identifies MMP1high basal cells derived from alveolar type II cells that contribute to microcyst formation in IPF, suggesting a therapeutic target through MMP inhibition or WNT modulation.

This study identifies LDHA-lactate-induced over-lactylation and TOP1 accumulation as drivers of PASMC hyper-proliferation and PAH, with TOP1 inhibition reversing these effects.

The paper shows MST1/2 promotes hyper-proliferation and apoptosis resistance in PAH pulmonary vascular cells by up-regulating CDC20.

This study shows that fibroblast proliferation drives pulmonary fibrosis and that targeting this process could be a new therapeutic strategy.

This study identifies β-III tubulin as a marker for anti-fibrotic pericytes in pulmonary fibrosis and shows that Tuj1-expressing pericytes release CXCL10 to inhibit pro-fibrotic macrophage differentiation.

The paper identifies a CD57+ cytotoxic CD8 T cell subset expanded in SSc-ILD patients and links it to lung injury through CD155-CD226 interactions.

This study shows PAI-1 deficiency in PASMC promotes pulmonary vascular remodeling and hypertension by enhancing uPA activity, leading to cell proliferation and reduced apoptosis.

This study investigates the association between mosaic loss of chromosome Y (mLOY) and pulmonary fibrosis, finding mLOY correlates with age and telomere length but not disease severity, and suggests a potential link between telomere shortening and mLOY.

This study identifies aging and senescence signatures in SSc-ILD through gene expression analysis and telomere length measurement, linking them to disease pathology.

The paper identifies a myeloid-mesenchymal crosstalk pathway involving Arg1 and ornithine that drives profibrotic metabolism in lung fibrosis.

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

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 shows mitochondrial activity and distribution are critical for cellular functions during alveolar formation, enabling secretion and migration necessary for alveoli development.

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