Idiopathic Pulmonary Fibrosis: Prevailing and Evolving Hypotheses about Its Pathogenesis and Implications for Therapy

By Moiss Selman, T. King, A. Pardo. Annals of Internal Medicine, 2001

1,825 citations recorded by the source corpus.

Subfields: Physiology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/919ae1708dac79a3762271557d9e29fbcd060370

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Physiology

1. TA Wynn
2. A. Luster

In Pulmonary and Respiratory Medicine

1. TA Wynn
2. G. Raghu
3. R. Mason
4. Zhi Zhang
5. T. Kamimura
6. H. Kasai
7. Jeremy T. Allen

Citations in the corpus

• Integrating mechanisms of pulmonary fibrosis (2011, background): “Idiopathic pulmonary fibrosis (IPF), a particularly severe form of pulmonary fibrosis with unknown etiology has a life expectancy of 2–6 yr after diagnosis (Selman et al., 2001).”
• Incidence and prevalence of idiopathic pulmonary fibrosis. (2006, background): “Its etiology is unknown, and the pathogenic mechanisms involved in its initiation and progression are poorly understood (1).”
• Interstitial lung disease guideline (2008, neutral): “Более того, эксперты не советуют назначать высокие дозы ГКС (преднизолон – 0,5– 1 мг/кг) больным с ИЛФ, у которых доказана ОИП или подтверждена при КТВР распространенная со товая дегенерация легочной ткани [45, 307, 312, 313].”
• The lysophosphatidic acid receptor LPA1 links pulmonary fibrosis to lung injury by mediating fibroblast recruitment and vascular leak (2008, background): “In the lung, aberrant wound-healing responses to injury are thought to contribute to the pathogenesis of idiopathic pulmonary fibrosis (IPF”
• TGF-β1 induces human alveolar epithelial to mesenchymal cell transition (EMT) (2005, background): “Background Idiopathic pulmonary fibrosis (IPF), the most common pulmonary fibrotic disorder, is a progressive and lethal disease of unknown etiology whose pathogenesis uniquely features the presence of fibroblastic foci in the parenchyma of the lungs [1].”
• Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression (2010, background): “The increases in stiffness far exceed previous macroscale measurements of fibrotic stiffening of the lung (Ebihara et al., 2000), and their highly localized nature is consistent with the patchy nature of both the bleomycin model and human disease (Selman et al., 2001; Moore and Hogaboam, 2008).”