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Evolving concepts of apoptosis in idiopathic pulmonary fibrosis.
Proc Am Thorac Soc 2006; 3(4):350-6PA

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic, relentlessly progressive fibrosing disease of the lung of unknown etiology. Significant progress has been made in recent years in elucidating key aspects of the pathobiology of IPF. Insights into disease pathogenesis have come from studies of cell biology, growth factor/cytokine signaling, animal models of pulmonary fibrosis, and human IPF cells and tissue. A consistent finding in the ultrastructural pathology of IPF is alveolar epithelial cell injury and apoptosis. Another consistent finding in the histopathology of human IPF, described as usual interstitial pneumonia, is the accumulation of aggregates of myofibroblasts in fibroblastic foci. The extent or profusion of fibroblastic foci in lung biopsies is strongly correlated with increased mortality in patients with IPF. There is emerging evidence that myofibroblasts in IPF/usual interstitial pneumonia, both in the in vivo microenvironment and during the process of differentiation in vitro, acquire resistance to apoptosis. Here, we review the current evidence and mechanisms for this apparent "apoptosis paradox" in the pathogenesis of IPF.

Authors+Show Affiliations

Division of Pulmonary and Critical Care Medicine, University of Michigan Medical Center, 6301 MSRB III, 1150 West Medical Center Drive, Ann Arbor, MI 48109, USA. vjt@umich.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

16738200

Citation

Thannickal, Victor J., and Jeffrey C. Horowitz. "Evolving Concepts of Apoptosis in Idiopathic Pulmonary Fibrosis." Proceedings of the American Thoracic Society, vol. 3, no. 4, 2006, pp. 350-6.
Thannickal VJ, Horowitz JC. Evolving concepts of apoptosis in idiopathic pulmonary fibrosis. Proc Am Thorac Soc. 2006;3(4):350-6.
Thannickal, V. J., & Horowitz, J. C. (2006). Evolving concepts of apoptosis in idiopathic pulmonary fibrosis. Proceedings of the American Thoracic Society, 3(4), pp. 350-6.
Thannickal VJ, Horowitz JC. Evolving Concepts of Apoptosis in Idiopathic Pulmonary Fibrosis. Proc Am Thorac Soc. 2006;3(4):350-6. PubMed PMID: 16738200.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Evolving concepts of apoptosis in idiopathic pulmonary fibrosis. AU - Thannickal,Victor J, AU - Horowitz,Jeffrey C, PY - 2006/6/2/pubmed PY - 2006/11/11/medline PY - 2006/6/2/entrez SP - 350 EP - 6 JF - Proceedings of the American Thoracic Society JO - Proc Am Thorac Soc VL - 3 IS - 4 N2 - Idiopathic pulmonary fibrosis (IPF) is a chronic, relentlessly progressive fibrosing disease of the lung of unknown etiology. Significant progress has been made in recent years in elucidating key aspects of the pathobiology of IPF. Insights into disease pathogenesis have come from studies of cell biology, growth factor/cytokine signaling, animal models of pulmonary fibrosis, and human IPF cells and tissue. A consistent finding in the ultrastructural pathology of IPF is alveolar epithelial cell injury and apoptosis. Another consistent finding in the histopathology of human IPF, described as usual interstitial pneumonia, is the accumulation of aggregates of myofibroblasts in fibroblastic foci. The extent or profusion of fibroblastic foci in lung biopsies is strongly correlated with increased mortality in patients with IPF. There is emerging evidence that myofibroblasts in IPF/usual interstitial pneumonia, both in the in vivo microenvironment and during the process of differentiation in vitro, acquire resistance to apoptosis. Here, we review the current evidence and mechanisms for this apparent "apoptosis paradox" in the pathogenesis of IPF. SN - 1546-3222 UR - https://www.unboundmedicine.com/medline/citation/16738200/Evolving_concepts_of_apoptosis_in_idiopathic_pulmonary_fibrosis_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/16738200/ DB - PRIME DP - Unbound Medicine ER -