Area of research
Pulmonary and Respiratory Medicine · Physiology
Research interest
Research interests include Chronic Obstructive Pulmonary Disease (COPD) Research, Neonatal Respiratory Health Research, Asthma and respiratory diseases, and Protease and Inhibitor Mechanisms.
Hypoxia Promotes the Expression of ADAM9 by Tubular Epithelial Cells, Which Enhances Transforming Growth Factor β1 Activation and Promotes Tissue Fibrosis in Patients With Lupus Nephritis.
Maternal smoking and CC-16: implications for lung development and COPD across the lifespan
A phase 1 study evaluating the safety, tolerability, and pharmacokinetics of the porcupine inhibitor, AZD5055
<i>Pseudomonas aeruginosa</i> infection is linked to increases in cardiovascular events post exacerbation in bronchiectasis.
ADAM9 promotes type I interferon-mediated innate immunity during encephalomyocarditis virus infection.
CC16 augmentation reduces exaggerated COPD-like disease in Cc16-deficient mice
CC16 augmentation reduces exaggerated COPD-like disease in Cc16-deficient mice
Loss of ADAM15 Exacerbates Transition to Decompensated Myocardial Hypertrophy and Dilation Through Activation of the Calcineurin Pathway.
Association of clonal hematopoiesis with chronic obstructive pulmonary disease.
ADAM15 is required for optimal collagen cross-linking and scar formation following myocardial infarction.
Association of clonal hematopoiesis with chronic obstructive pulmonary disease
Metformin: Experimental and Clinical Evidence for a Potential Role in Emphysema Treatment
Long-term safety and efficacy of tezacaftor–ivacaftor in individuals with cystic fibrosis aged 12 years or older who are homozygous or heterozygous for Phe508del CFTR (EXTEND): an open-label extension study
A phase 3, double-blind, parallel-group study to evaluate the efficacy and safety of tezacaftor in combination with ivacaftor in participants 6 through 11 years of age with cystic fibrosis homozygous for F508del or heterozygous for the F508del-CFTR mutation and a residual function mutation.
Hedgehog interacting protein (HHIP) represses airway remodeling and metabolic reprogramming in COPD-derived airway smooth muscle cells
A disintegrin and metalloproteinase domain-15 deficiency leads to exaggerated cigarette smoke-induced chronic obstructive pulmonary disease (COPD)-like disease in mice.
Surface-bound matrix metalloproteinase-8 on macrophages: Contributions to macrophage pericellular proteolysis and migration through tissue barriers.
ADAM15 expression is increased in lung CD8<sup>+</sup> T cells, macrophages, and bronchial epithelial cells in patients with COPD and is inversely related to airflow obstruction.
"T"eeing Up A Novel Therapy for Lymphangioleiomyomatosis.
CFTR regulates B cell activation and lymphoid follicle development
Tissue Inhibitor of Metalloproteinase-1 Promotes Polymorphonuclear Neutrophil (PMN) Pericellular Proteolysis by Anchoring Matrix Metalloproteinase-8 and -9 to PMN Surfaces.
Dusting Off IL-9 as a New Therapeutic Target for Pulmonary Fibrosis.
Endothelial Cell Death in Emphysema: More Sugarcoating Needed?
To Bet or Not to Bet on T-bet As a Therapeutic Target in Emphysema?
Mitochondrial Dysfunction as a Pathogenic Mediator of Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis
Club Cell Secretory Protein Deficiency Leads to Altered Lung Function
Matrix metalloproteinase-9 deficiency protects mice from severe influenza A viral infection
A Disintegrin and Metalloproteinase Domain-8: A Novel Protective Proteinase in Chronic Obstructive Pulmonary Disease
A Disintegrin and Metalloproteinase Domain-9: A Novel Proteinase Culprit with Multifarious Contributions to Chronic Obstructive Pulmonary Disease
A Pilot Study Linking Endothelial Injury in Lungs and Kidneys in Chronic Obstructive Pulmonary Disease