Timothy S. Blackwell

Integrin α3β1 is required for alveolar-capillary barrier formation through regulation of epithelial differentiation

This study shows that integrin α3β1 is essential for alveolar-capillary barrier formation by regulating epithelial differentiation during lung development.

Clade B serpins promote direct basal-to-goblet cell differentiation in airways of patients with chronic obstructive pulmonary disease

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.

Sustained Yap/Taz activation promotes aberrant alveolar epithelial cell differentiation and drives persistent fibrotic remodeling

This study shows sustained Yap/Taz activation in alveolar epithelial cells leads to fibrotic remodeling and impaired repair, with potential therapeutic implications.

Longitudinal Single-Cell RNA-seq Profiling of Lung Cell Phenotypes, Signaling, and Cross-talk During Fibrosis Resolution

The paper uses longitudinal single-cell RNA-seq to study lung fibrosis resolution, identifying pro- and anti-fibrotic pathways and cellular interactions during recovery.

T-cell Multiomic Analysis Identifies Subsets and Mechanisms of Interaction with Epithelial Cells in Idiopathic Pulmonary Fibrosis

The paper identifies T-cell subsets and their interactions with epithelial cells in IPF using multiomic profiling, revealing novel signaling pathways and activation patterns.

Loss of Regulator of telomere elongation helicase (Rtel1) impairs alveolar epithelial cell progenitor function but does not exacerbate experimental fibrosis

This study shows RTEL1 regulates alveolar epithelial cell progenitor function but does not worsen experimental lung fibrosis in mice.

Accelerated Biological Aging in Familial Pulmonary Fibrosis

This study finds accelerated epigenetic aging in individuals at-risk for familial pulmonary fibrosis and patients, independent of telomere-related genetic variants or telomere length.

Image-based spatial transcriptomics identifies molecular niche dysregulation associated with distal lung remodeling in pulmonary fibrosis

Xenium profiling of 343 genes in 1,126,820 nuclei from 19 human lungs maps fibrosis niches and orders alveolar remodeling from alveolar-capillary disruption to SPP1+ macrophage accumulation.

Rare variants and survival of patients with idiopathic pulmonary fibrosis

This study investigates the impact of rare variants and polygenic risk scores on survival in idiopathic pulmonary fibrosis patients, finding that rare variants are associated with worse outcomes.

Cell type-specific and disease-associated eQTL in the human lung

The paper identifies cell-type-specific and disease-associated eQTL in the human lung using single-cell RNA-sequencing data from PF and unaffected donors.

PCSK6 and Survival in Idiopathic Pulmonary 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.

Epithelial Outgrowth Through Mesenchymal Rings Drives Alveologenesis

The paper observes alveoli formation through epithelial outgrowth and mesenchymal rings in live lung slices, challenging the existing model of airspace subdivision.

A Single Cell Atlas of Lung Development

The paper constructs a single-cell RNA sequencing atlas of lung development in mice, revealing cellular dynamics and transcriptional changes during the saccular to alveolar transition.

Age-related expression of SARS-CoV-2 priming protease TMPRSS2 in the developing lung

The paper identifies TMPRSS2 expression patterns in developing lungs and links them to SARS-CoV-2 infection susceptibility in different age groups.

Single-cell RNA-sequencing reveals profibrotic roles of distinct epithelial and mesenchymal lineages in pulmonary fibrosis

Single-cell RNA-sequencing identifies distinct epithelial and mesenchymal cell types and their roles in pulmonary fibrosis.

Comprehensive Analysis of Constraint on the Spatial Distribution of Missense Variants in Human Protein Structures

The paper analyzes the spatial distribution of missense variants in human protein structures to classify variants of unknown significance, finding disease-causing variants cluster more than benign ones.