The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Alveolar lipids in pulmonary disease. A review
Open accessAbstract
Lung lipid metabolism participates both in infant and adult pulmonary disease. The lung is composed by multiple cell types with specialized functions and coordinately acting to meet specific physiologic requirements. The alveoli are the niche of the most active lipid metabolic cell in the lung, the type 2 cell (T2C). T2C synthesize surfactant lipids that are an absolute requirement for respiration, including dipalmitoylphosphatidylcholine. After its synthesis and secretion into the alveoli, surfactant is recycled by the T2C or degraded by the alveolar macrophages (AM). Surfactant biosynthesis and recycling is tightly regulated, and dysregulation of this pathway occurs in many pulmonary disease processes. Alveolar lipids can participate in the development of pulmonary disease from their extracellular location in the lumen of the alveoli, and from their intracellular location in T2C or AM. External insults like smoke and pollution can disturb surfactant homeostasis and result in either surfactant insufficiency or accumulation. But disruption of surfactant homeostasis is also observed in many chronic adult diseases, including chronic obstructive pulmonary disease (COPD), and others. Sustained damage to the T2C is one of the postulated causes of idiopathic pulmonary fibrosis (IPF), and surfactant homeostasis is disrupted during fibrotic conditions. Similarly, surfactant homeostasis is impacted during acute respiratory distress syndrome (ARDS) and infections. Bioactive lipids like eicosanoids and sphingolipids also participate in chronic lung disease and in respiratory infections. We review the most recent knowledge on alveolar lipids and their essential metabolic and signaling functions during homeostasis and during some of the most commonly observed pulmonary diseases.
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
Reyfman, P. A., Walter, J. M., Joshi, N., Anekalla, K. R., McQuattie-Pimentel, A. C., Chiu, S., Fernandez, R., Akbarpour, M., Chen, C.-I., Ren, Z., et al. (2019) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201712-2410oc · Cited by 1,203
Alveolar epithelial type II cell: defender of the alveolus revisited
Fehrenbach, H. (2001) · Respiratory Research · doi:10.1186/rr36 · Cited by 757 · cited 1×
“T2C contribute to other essential roles for pulmonary homeostasis and alveolar repair [82], as well as in immune defense processes [83] and inflammation [84, 85].”
BackgroundAlveolar Cell Senescence in Patients with Pulmonary Emphysema
Tsuji, T., Aoshiba, K., & Nagai, A. (2006) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200509-1374oc · Cited by 527
Hodge, S., Hodge, G., Scicchitano, R., Reynolds, P. N., & Holmes, M. (2003) · Immunology & Cell Biology · doi:10.1046/j.1440-1711.2003.t01-1-01170.x · Cited by 440 · cited 1×
“Efferocytosis is necessary for elimination of airway apoptotic cells that if not removed, can eventually necrotize and lead to chronic inflammation [112].”
BackgroundGünther, A., Siebert, C., Schmidt, R., Ziegler, S., Grimminger, F., Yabut, M., Temmesfeld, B., Walmrath, D., Morr, H., & Seeger, W. (1996) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/ajrccm.153.1.8542113 · Cited by 417
Telomere dysfunction causes alveolar stem cell failure
Alder, J. K., Barkauskas, C. E., Limjunyawong, N., Stanley, S. E., Kembou, F., Tuder, R. M., Hogan, B. L. M., Mitzner, W., & Armanios, M. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1504780112 · Cited by 339
Kolodsick, J. E., Peters-Golden, M., Larios, J., Toews, G. B., Thannickal, V. J., & Moore, B. B. (2003) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2002-0243oc · Cited by 294
The Human Lung Cell Atlas: A High-Resolution Reference Map of the Human Lung in Health and Disease
Schiller, H. B., Montoro, D. T., Simon, L. M., Rawlins, E. L., Meyer, K. B., Strunz, M., Vieira Braga, F. A., Timens, W., Koppelman, G. H., Budinger, G. R. S., et al. (2019) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2018-0416tr · Cited by 245
Mice with Pulmonary Fibrosis Driven by Telomere Dysfunction
Povedano, J. M., Martinez, P., Flores, J. M., Mulero, F., & Blasco, M. A. (2015) · Cell Reports · doi:10.1016/j.celrep.2015.06.028 · Cited by 225 · cited 2×
“DNA damage and telomere shortening in T2C induced pulmonary fibrosis and decrease survival in mice [135] (Table 1).”
BackgroundThe heterogeneity of lung macrophages in the susceptibility to disease
Morales-Nebreda, L., Misharin, A. V., Perlman, H., & Budinger, G. R. S. (2015) · European Respiratory Review · doi:10.1183/16000617.0031-2015 · Cited by 162
Cited by
Understanding of COVID‐19 based on current evidence
Sun, P., Lu, X., Xu, C., Sun, W., & Pan, B. (2020) · Journal of Medical Virology · doi:10.1002/jmv.25722 · Cited by 1,107
Aboudounya, M. M., & Heads, R. J. (2021) · Mediators of Inflammation · doi:10.1155/2021/8874339 · Cited by 346
Metadata
- Authors
- Agudelo, C. W., Samaha, G., & Garcia-Arcos, I.
- Venue
- Lipids in Health and Disease
- Published
- 2020-06-03
- Volume
- 19
- Issue
- 1
- Pages
- 122-122
- ISSN
- 1476-511X (ISSN-L)
- OpenAlex
- W3029626770
- Cited by
- 202
- References
- 12
- FWCI
- 12.19
- 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: Alveolar lipids in pulmonary disease. A review. https://app.cochat.ai/papers/10.1186/s12944-020-01278-8
- The paper
- Agudelo, C. W., Samaha, G., & Garcia-Arcos, I. (2020). Alveolar lipids in pulmonary disease. A review. Lipids in Health and Disease. https://doi.org/10.1186/s12944-020-01278-8
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.