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Cited by 364

The DOI matches its Crossref record; 68 of the 68 references it cites were found in a registry or an index.

Evolving Concepts of Apoptosis in Idiopathic Pulmonary Fibrosis

Open access
Thannickal, Victor J., Horowitz, Jeffrey C.·2006·Proceedings of the American Thoracic Society
DOI 10.1513/pats.200601-001tk
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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.

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Metadata

Authors
Thannickal, V. J., & Horowitz, J. C.
Venue
Proceedings of the American Thoracic Society
Publisher
Oxford University Press (OUP)
Published
2006-06-01
Volume
3
Issue
4
Pages
350-356
ISSN
  • 1546-3222 (ISSN-L)
  • 1943-5665
DOI
10.1513/pats.200601-001tk
OpenAlex
W2111223419
Cited by
364
References
68
FWCI
13.42
Type
journal article
Language
en
Open access
green

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

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