The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
New Therapeutic Targets in Idiopathic Pulmonary Fibrosis. Aiming to Rein in Runaway Wound-Healing Responses
Open accessAbstract
Idiopathic pulmonary fibrosis (IPF) is a devastating disease, with a median survival as short as 3 years from the time of diagnosis and no pharmacological therapies yet approved by the U.S. Food and Drug Administration. To address the great unmet need for effective IPF therapy, a number of new drugs have recently been, or are now being, evaluated in clinical trials. The rationales for most of these therapeutic candidates are based on the current paradigm of IPF pathogenesis, in which recurrent injury to the alveolar epithelium is believed to drive aberrant wound healing responses, resulting in fibrosis rather than repair. Here we discuss drugs in recently completed or currently ongoing phase II and III IPF clinical trials in the context of their putative mechanisms of action and the aberrant repair processes they are believed to target: innate immune activation and polarization, fibroblast accumulation and myofibroblast differentiation, or extracellular matrix deposition and stiffening. Placed in this context, the positive results of recently completed trials of pirfenidone and nintedanib, and results that will come from ongoing trials of other agents, should provide valuable insights into the still-enigmatic pathogenesis of this disease, in addition to providing benefits to patients with IPF.
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Cites
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Protective and pathogenic functions of macrophage subsets
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Efficacy and Safety of Nintedanib in Idiopathic Pulmonary Fibrosis
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Tumors: Wounds That Do Not Heal
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“inflammatory cells, new blood vessels, and fibroblasts migrate (28).”
BackgroundInfluentialA phase 3 trial of pirfenidone in patients with idiopathic pulmonary fibrosis.
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Telomerase Mutations in Families with Idiopathic Pulmonary Fibrosis
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Cited by
Tsukui, T., Sun, K.-H., Wetter, J. B., Wilson-Kanamori, J. R., Hazelwood, L. A., Henderson, N. C., Adams, T. S., Schupp, J. C., Poli, S. D., Rosas, I. O., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-15647-5 · Cited by 765
TGF-β1 Signaling and Tissue Fibrosis
Kim, K. K., Sheppard, D., & Chapman, H. A. (2018) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a022293 · Cited by 800
Extracellular matrix as a driver of progressive fibrosis
Herrera, J., Henke, C. A., & Bitterman, P. B. (2018) · Journal of Clinical Investigation · doi:10.1172/jci93557 · Cited by 615
Extracellular matrix in lung development, homeostasis and disease
Zhou, Y., Horowitz, J. C., Naba, A., Ambalavanan, N., Atabai, K., Balestrini, J., Bitterman, P. B., Corley, R. A., Ding, B.-S., Engler, A. J., et al. (2018) · Matrix Biology · doi:10.1016/j.matbio.2018.03.005 · Cited by 284
The extracellular matrix – the under‐recognized element in lung disease?
Burgess, J. K., Mauad, T., Tjin, G., Karlsson, J. C., & Westergren‐Thorsson, G. (2016) · The Journal of Pathology · doi:10.1002/path.4808 · Cited by 266
Metadata
- Authors
- Ahluwalia, N., Shea, B. S., & Tager, A. M.
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-10-15
- Volume
- 190
- Issue
- 8
- Pages
- 867-878
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W2045730105
- Cited by
- 235
- References
- 33
- FWCI
- 20.35
- Type
- journal article
- Language
- en
- Open access
- green
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- Ahluwalia, N., Shea, B. S., & Tager, A. M. (2014). New Therapeutic Targets in Idiopathic Pulmonary Fibrosis. Aiming to Rein in Runaway Wound-Healing Responses. American Journal of Respiratory and Critical Care Medicine. https://doi.org/10.1164/rccm.201403-0509pp
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