The DOI matches its Crossref record; 104 of the 104 references it cites were found in a registry or an index.
Revealing the Pathogenic and Aging-related Mechanisms of the Enigmatic Idiopathic Pulmonary Fibrosis. An Integral Model
Abstract
A growing body of evidence indicates that aberrant activation of alveolar epithelial cells and fibroblasts in an aging lung plays a critical role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, the biopathological processes linking aging with IPF and the mechanisms responsible for the abnormal activation of epithelial cells and fibroblasts have not been elucidated. Many of the hallmarks of aging (e.g., genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, and cellular senescence) have been proposed as essential mechanisms for the development of IPF; however, these disturbances are not restricted to IPF and also occur in other aging-related lung disorders, primarily chronic obstructive pulmonary disease (COPD). Therefore, an unanswered question is why a current/former smoker of about 60 years of age with shorter telomeres, alveolar epithelial senescence, excessive oxidative stress, and mitochondrial dysfunction develops IPF and not COPD; in other words, what makes old lungs specifically susceptible to develop IPF? In this Perspective, we propose an integral model in which the combination of some gene variants and/or gene expression in the aging lung results in the loss of epithelial integrity and consequently in the failure of the alveoli to correctly respond to injury and to face the stress associated with mechanical stretch. Afterward, a distinctive epigenetic "reprogramming" that affects both epithelial cells and fibroblasts provokes, among others, the recapitulation of developmental pathways and the aberrant activation and miscommunication between both cell types, resulting in the exaggerated production and accumulation of extracellular matrix and the subsequent destruction of the lung architecture.
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
López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013) · Cell · doi:10.1016/j.cell.2013.05.039 · Cited by 14,982
King, T. E., Pardo, A., & Selman, M. (2011) · The Lancet · doi:10.1016/s0140-6736(11)60052-4 · Cited by 2,194
Self-citationIncidence and Prevalence of Idiopathic Pulmonary Fibrosis
Raghu, G., Weycker, D., Edelsberg, J., Bradford, W. Z., & Oster, G. (2006) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200602-163oc · Cited by 1,310
Pathophysiology of airflow limitation in chronic obstructive pulmonary disease
Hogg, J. C. (2004) · The Lancet · doi:10.1016/s0140-6736(04)16900-6 · Cited by 1,294
Rock, J. R., Barkauskas, C. E., Cronce, M. J., Xue, Y., Harris, J. R., Liang, J., Noble, P. W., & Hogan, B. L. M. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1117988108 · Cited by 1,030
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
Genome-wide association study identifies multiple susceptibility loci for pulmonary fibrosis
Fingerlin, T. E., Murphy, E., Zhang, W., Peljto, A. L., Brown, K. K., Steele, M. P., Loyd, J. E., Cosgrove, G. P., Lynch, D., Groshong, S., et al. (2013) · Nature Genetics · doi:10.1038/ng.2609 · Cited by 809
Self-citationShort telomeres are a risk factor for idiopathic pulmonary fibrosis
Alder, J. K., Chen, J. J.-L., Lancaster, L., Danoff, S., Su, S.-C., Cogan, J. D., Vulto, I., Xie, M., Qi, X., Tuder, R. M., et al. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0804280105 · Cited by 805
Pillai, S. G., Ge, D., Zhu, G., Kong, X., Shianna, K. V., Need, A. C., Feng, S., Hersh, C. P., Bakke, P., Gulsvik, A., et al. (2009) · PLoS Genetics · doi:10.1371/journal.pgen.1000421 · Cited by 777
Kirkham, P. A., & Barnes, P. J. (2013) · Chest · doi:10.1378/chest.12-2664 · Cited by 685
Cited by
Lederer, D. J., & Martinez, F. J. (2018) · New England Journal of Medicine · doi:10.1056/nejmra1705751 · Cited by 2,056
Martinez, F. J., Collard, H. R., Pardo, A., Raghu, G., Richeldi, L., Selman, M., Swigris, J. J., Taniguchi, H., & Wells, A. U. (2017) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2017.74 · Cited by 1,388
Self-citationCho, S. J., & Stout-Delgado, H. W. (2020) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021119-034610 · Cited by 458
IPF lung fibroblasts have a senescent phenotype
Álvarez, D., Cárdenes, N., Sellarés, J., Bueno, M., Corey, C., Hanumanthu, V. S., Peng, Y., D’Cunha, H., Sembrat, J., Nouraie, M., et al. (2017) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00220.2017 · Cited by 342
Meiners, S., Eickelberg, O., & Königshoff, M. (2015) · European Respiratory Journal · doi:10.1183/09031936.00186914 · Cited by 340
Metadata
- Authors
- Selman, M., & Pardo, A.
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2014-05-15
- Volume
- 189
- Issue
- 10
- Pages
- 1161-1172
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W2162175607
- Cited by
- 454
- References
- 104
- FWCI
- 27.38
- Type
- journal article
- Language
- en
- Open access
- closed
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: Revealing the Pathogenic and Aging-related Mechanisms of the Enigmatic Idiopathic Pulmonary Fibrosis. An Integral Model. https://app.cochat.ai/papers/10.1164/rccm.201312-2221pp
- The paper
- Selman, M., & Pardo, A. (2014). Revealing the Pathogenic and Aging-related Mechanisms of the Enigmatic Idiopathic Pulmonary Fibrosis. An Integral Model. American Journal of Respiratory and Critical Care Medicine. https://doi.org/10.1164/rccm.201312-2221pp
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.
