Edward P. Manning

This study shows that a single crystalline silica exposure causes subclinical cardiopulmonary abnormalities in mice, with sex-dependent effects on lung mechanics and transcriptomic responses.

This study compares in vivo and ex vivo lung biomechanics in mice, finding that thoracic structures mainly affect dynamic dissipation and heterogeneity rather than intrinsic elastic properties.

The paper develops a multimodal model to predict biological age using vascular microstructure and biomechanical parameters in mice, achieving high predictive accuracy.

The paper presents data on normal postnatal development of pulmonary arteries in mice and develops a computational model to simulate responses to hemodynamic perturbations.

This study quantifies biological cardiopulmonary aging in mice by integrating biomechanics and single-cell transcriptomics, revealing non-linear aging patterns and cell-type-specific gene expression changes.

The paper identifies a conserved tissue-level stress response to proteolytic damage, characterized by heme release and oxidative stress, and shows how alveolar macrophages and fibroblasts respond to mitigate damage.

This study identifies early alveolar niche disruption and aberrant epithelial reprogramming in IPF using multi-modal analyses of patient cohorts.

This study evaluates modified RNA extraction methods to remove agarose impurities from precision-cut lung slices, showing improved RNA quantity and integrity using a plant kit and agarose dissolution.

The paper investigates age-related changes in proximal pulmonary artery mechanics in mouse models, finding increased stiffness and collagen reorientation linked to aging biomarkers and cellular senescence.

This study shows that EGFR regulates Beclin-1 and autophagy in hyperoxic acute lung injury, suggesting a novel therapeutic pathway.

This study introduces CausaLink, a cross-scale causal mapping framework that identifies Mgl2 macrophages as key regulators of balanced arterial development using single-cell transcriptomics and organoid validation.

The paper investigates growth arrest in thoracic aortic aneurysms of aging Marfan mice, identifying gene expression and proteomic changes that may contribute to disease stabilization.

This study examines hypoxia-induced cardiopulmonary remodeling in mice, finding that pulmonary artery stiffening due to collagen remodeling precedes and correlates with cardiac and lung dysfunction, with partial recovery observed after normoxia.

This study investigates GPR87's role in pulmonary fibrosis, finding it highly expressed in IPF lungs and protective against fibrosis when knocked down in multiple models.

This study uses multi-omic data to identify age-related changes in lung cell composition and molecular programs associated with aging and senescence.