The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
The pathogenesis of COPD and IPF: Distinct horns of the same devil?
Open accessAbstract
New paradigms have been recently proposed in the pathogenesis of both chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), evidencing surprising similarities between these deadly diseases, despite their obvious clinical, radiological and pathologic differences. There is growing evidence supporting a "double hit" pathogenic model where in both COPD and IPF the cumulative action of an accelerated senescence of pulmonary parenchyma (determined by either telomere dysfunction and/or a variety of genetic predisposing factors), and the noxious activity of cigarette smoke-induced oxidative damage are able to severely compromise the regenerative potential of two pulmonary precursor cell compartments (alveolar epithelial precursors in IPF, mesenchymal precursor cells in COPD/emphysema). The consequent divergent derangement of signalling pathways involved in lung tissue renewal (mainly Wnt and Notch), can eventually lead to the distinct abnormal tissue remodelling and functional impairment that characterise the alveolar parenchyma in these diseases (irreversible fibrosis and bronchiolar honeycombing in IPF, emphysema and airway chronic inflammation in COPD).
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Vestbo, J., Hurd, S. S., Agustí, A. G., Jones, P. W., Vogelmeier, C., Anzueto, A., Barnes, P. J., Fabbri, L. M., Martinez, F. J., Nishimura, M., et al. (2013) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201204-0596pp · Cited by 15,983
The senescence-associated secretory phenotype: the dark side of tumor suppression
Coppé, J.-P., Desprez, P.-Y., Krtolica, A., & Campisi, J. (2010) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-121808-102144 · Cited by 5,206
Human mesenchymal stem cells modulate allogeneic immune cell responses
Aggarwal, S., & Pittenger, M. F. (2005) · Blood · doi:10.1182/blood-2004-04-1559 · Cited by 4,511
King, T. E., Pardo, A., & Selman, M. (2011) · The Lancet · doi:10.1016/s0140-6736(11)60052-4 · Cited by 2,194
Telomerase Mutations in Families with Idiopathic Pulmonary Fibrosis
Armanios, M. Y., Chen, J. J.-L., Cogan, J. D., Alder, J. K., Ingersoll, R. G., Markin, C., Lawson, W. E., Xie, M., Vulto, I., Phillips, J. A., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa066157 · Cited by 1,357
miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis
Liu, G., Friggeri, A., Yang, Y., Milosevic, J., Ding, Q., Thannickal, V. J., Kaminski, N., & Abraham, E. (2010) · Journal of Experimental Medicine · doi:10.1084/jem.20100035 · Cited by 935
A Mutation in the Surfactant Protein C Gene Associated with Familial Interstitial Lung Disease
Nogee, L. M., Dunbar, A. E., Wert, S. E., Askin, F., Hamvas, A., & Whitsett, J. A. (2001) · New England Journal of Medicine · doi:10.1056/nejm200102223440805 · Cited by 929
Adult-onset pulmonary fibrosis caused by mutations in telomerase
Tsakiri, K. D., Cronkhite, J. T., Kuan, P. J., Xing, C., Raghu, G., Weissler, J. C., Rosenblatt, R. L., Shay, J. W., & Garcia, C. K. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0701009104 · Cited by 894 · cited 1×
“senescence and lung “premature aging” [19-33].”
p63 Is Essential for the Proliferative Potential of Stem Cells in Stratified Epithelia
Senoo, M., Pinto, F., Crum, C. P., & McKeon, F. (2007) · Cell · doi:10.1016/j.cell.2007.02.045 · Cited by 881
Augmented Wnt signaling in a mammalian model of accelerated aging
Liu, H., Fergusson, M. M., Castilho, R. M., Liu, J., Cao, L., Chen, J., Malide, D., Rovira, I. I., Schimel, D., Kuo, C. J., et al. (2007) · Science · doi:10.1126/science.1143578 · Cited by 755 · cited 1×
“In line with this assumption, both Wnt- and Notch pathways have been shown to be activated by cell senescence, and epithelial mesenchymal transition and mobilization of beta-catenin are among the features characterising the senescence-related hypersecretive phenotype [88-95].”
Cited by
Nilius, B., & Szallasi, A. (2014) · Pharmacological Reviews · doi:10.1124/pr.113.008268 · Cited by 506
COPDGene Investigators, Hobbs, B. D., ECLIPSE Investigators, LifeLines Investigators, SPIROMICS Research Group, International COPD Genetics Network Investigators, UK BiLEVE Investigators, International COPD Genetics Consortium, de Jong, K., Lamontagne, M., et al. (2017) · Nature Genetics · doi:10.1038/ng.3752 · Cited by 398
Sakornsakolpat, P., Prokopenko, D., Lamontagne, M., Reeve, N. F., Guyatt, A. L., Jackson, V. E., Shrine, N., Qiao, D., Bartz, T. M., Kim, D. K., et al. (2019) · Nature Genetics · doi:10.1038/s41588-018-0342-2 · Cited by 384
Genome-wide association study of susceptibility to idiopathic pulmonary fibrosis
Allen, R. J., Guillen-Guio, B., Oldham, J. M., Ma, S.-F., Dressen, A., Paynton, M. L., Kraven, L. M., Obeidat, M., Li, X., Ng, M., et al. (2020) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201905-1017oc · Cited by 329
Chilosi, M., Carloni, A., Rossi, A., & Poletti, V. (2013) · Translational Research · doi:10.1016/j.trsl.2013.06.004 · Cited by 317
Self-citation
Metadata
- Authors
- Chilosi, M., Poletti, V., & Rossi, A.
- Venue
- Respiratory Research
- Published
- 2012
- Volume
- 13
- Issue
- 1
- Pages
- 3
- ISSN
- 1465-9921 (ISSN-L)
- OpenAlex
- W2117918359
- Cited by
- 183
- References
- 26
- FWCI
- 12.33
- Type
- journal article
- Language
- en
- Open access
- gold
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: The pathogenesis of COPD and IPF: Distinct horns of the same devil? https://app.cochat.ai/papers/10.1186/1465-9921-13-3
- The paper
- Chilosi, M., Poletti, V., & Rossi, A. (2012). The pathogenesis of COPD and IPF: Distinct horns of the same devil? Respiratory Research. https://doi.org/10.1186/1465-9921-13-3
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
