- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Pulmonary Hypertension Research and Treatments
- Medical Imaging and Pathology Studies
- Chronic Obstructive Pulmonary Disease (COPD) Research
- Neonatal Respiratory Health Research
- Protease and Inhibitor Mechanisms
- Occupational and environmental lung diseases
- Occupational exposure and asthma
- Peptidase Inhibition and Analysis
- Inhalation and Respiratory Drug Delivery
- Sarcoidosis and Beryllium Toxicity Research
- Extracellular vesicles in disease
- Fibroblast Growth Factor Research
- Connective tissue disorders research
- Immune Cell Function and Interaction
- Pleural and Pulmonary Diseases
- IL-33, ST2, and ILC Pathways
- Pneumonia and Respiratory Infections
- Proteoglycans and glycosaminoglycans research
- MicroRNA in disease regulation
- Pediatric health and respiratory diseases
- Autophagy in Disease and Therapy
- Collagen: Extraction and Characterization
- Cardiac Fibrosis and Remodeling
- Systemic Sclerosis and Related Diseases
Georg Speyer Haus
2025
Universidad Nacional Autónoma de México
2015-2024
Instituto Nacional de Enfermedades Respiratorias
2001-2020
American Thoracic Society
2017
University of Michigan
2017
Laboratoire de Biochimie
2016
National Institute of Cardiovascular Diseases
2015
Harvard University
2011
Northwestern University
2009
University of Pittsburgh
2008
Pulmonary fibrosis is a progressive and largely untreatable group of disorders that affects up to 100,000 people on any given day in the United States. To elucidate molecular mechanisms lead end-stage human pulmonary we analyzed samples from patients with histologically proven (usual interstitial pneumonia) by using oligonucleotide microarrays. Gene expression patterns clearly distinguished normal fibrotic lungs. Many genes were significantly increased lungs encoded proteins associated...
Background Idiopathic pulmonary fibrosis (IPF) is a chronic progressive fibrotic lung disease associated with substantial morbidity and mortality. The objective of this study was to determine whether there peripheral blood protein signature in IPF components may serve as biomarkers for presence progression. Methods Findings We analyzed the concentrations 49 proteins plasma 74 patients 53 control individuals. identified combinatorial five proteins—MMP7, MMP1, MMP8, IGFBP1, TNFRSF1A—that...
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and usually lethal fibrotic lung disease characterized by profound changes in epithelial cell phenotype fibroblast proliferation.To determine expression role of microRNAs IPF.RNA from 10 control IPF tissues was hybridized on Agilent microRNA microarrays results were confirmed quantitative real-time polymerase chain reaction situ hybridization. SMAD3 binding to the let-7d promoter chromatin immunoprecipitation, electrophoretic...
Background Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disorder characterized by fibroproliferation excessive accumulation of extracellular matrix in the lung. Methods Findings Using oligonucleotide arrays, we identified osteopontin as one genes that significantly distinguishes IPF from normal lungs. Osteopontin was localized to alveolar epithelial cells lungs also elevated bronchoalveolar lavage patients. To study fibrosis-relevant effects stimulated primary human lung...
Many of the interstitial lung diseases represent a diagnostic and therapeutic challenge because their clinical even histologic features are often nonspecific. Likewise, transcriptional signatures most them unknown.To compare gene expression patterns from patients with idiopathic pulmonary fibrosis (IPF) hypersensitivity pneumonitis (HP), nonspecific pneumonia (NSIP) using custom oligonucleotide microarrays.We profiled biopsies 15 IPF, 12 HP, eight NSIP. Labeled complementary ribonucleic acid...
A growing body of evidence indicates that aberrant activation alveolar epithelial cells and fibroblasts in an aging lung plays a critical role the pathogenesis idiopathic pulmonary fibrosis (IPF). However, biopathological processes linking with IPF mechanisms responsible for abnormal have not been elucidated. Many hallmarks (e.g., genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, cellular senescence) proposed as essential development IPF; however,...
Fibroblast proliferation and extracellular matrix accumulation characterize idiopathic pulmonary fibrosis (IPF). We evaluated the presence of tissue inhibitor metalloproteinase (TIMP)-1, -2, -3, -4; collagenase-1, -3; gelatinases A B; membrane type 1 (MMP) in 12 IPF 6 control lungs. TIMP-1 was found interstitial macrophages TIMP-2 fibroblast foci. TIMP-3 revealed an intense staining mainly decorating elastic lamina vessels. TIMP-4 expressed lungs by epithelial plasma cells. colocalized with...
Numerous compounds have shown efficacy in limiting development of pulmonary fibrosis using animal models, yet few these replicated beneficial effects clinical trials. Given the challenges associated with performing trials patients idiopathic (IPF), it is imperative that preclinical data packages be robust their analyses and interpretations to best chance selecting promising drug candidates advance The American Thoracic Society has convened a group experts lung discuss formalize...
The authors discuss evidence suggesting that embryonic signaling pathways involved in epithelium/mesenchymal communication and epithelial cell plasticity may be aberrantly switched on idiopathic pulmonary fibrosis.
Rationale: Idiopathic pulmonary fibrosis (IPF) is a rare, irreversible, and progressive disease of the lungs. Common genetic variants, in addition to nongenetic factors, have been consistently associated with IPF. Rare variants identified by candidate gene, family-based, exome studies also reported associate However, extent which rare genome-wide, may contribute risk IPF remains unknown. Objectives: We used whole-genome sequencing investigate role on risk. Methods: As part Trans-Omics for...