The role of MIF in chronic lung diseases: looking beyond inflammation
Open accessAbstract
Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that has been associated with many diseases. Most studies found in literature describe MIF as a proinflammatory cytokine involved in chronic inflammatory conditions, but evidence from last years suggests that many of its key effects are not directly related to inflammation. In fact, MIF is constitutively expressed in most human tissues and in some cases in high levels, which does not reflect the pattern of expression of a classic proinflammatory cytokine. Moreover, MIF is highly expressed during embryonic development and decreases during adulthood, which point toward a more likely role as growth factor. Accordingly, MIF knockout mice develop age-related spontaneous emphysema, suggesting that MIF presence (e.g., in younger individuals and wild-type animals) is part of a healthy lung. In view of this new line of evidence, we aimed to review data on the role of MIF in the pathogenesis of chronic lung diseases.
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MIF appears to be pivotal for cellular senescence, aging, and joint inflammation; however, its presence has been associated with a beneficial effect on the healthy lung and in MSCs.
“MIF appears to be pivotal for cellular senescence, aging, and joint inflammation; however, its presence has been associated with a beneficial effect on the healthy lung and in MSCs73–78.”
From A new gene set identifies senescent cells and predicts senescence-associated pathways across tissues (2022) · cites this paper as [76]
The review links MIF to aging and cellular senescence and says it may protect the lung from senescence and damage (MIF IN CHRONIC LUNG DISEASES, p. 3). Its table also lists a protective effect in mesenchymal stem cells (CHRONIC LUNG DISEASES AND MIF, p. 5). The passages do not establish the claim about joint inflammation. (LLM, conf=0.85)
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Jalce, G., & Guignabert, C. (2019) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00234.2019 · Cited by 20 · see citing works
Wang, Q., Wei, Y., & Zhang, J. (2017) · International Journal of Gynecological Cancer · doi:10.1097/igc.0000000000000951 · Cited by 19 · see citing works
MiR-608 exerts tumor suppressive function in lung adenocarcinoma by directly targeting MIF.
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Reprint of: The non-mammalian MIF superfamily
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Corallo, C., Paulesu, L. R., Cutolo, M., et al. (2015) · PubMed · Cited by 13 · see citing works
Role of MIF/CD74 signaling pathway in the development of pleural mesothelioma
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A new gene set identifies senescent cells and predicts senescence-associated pathways across tissues
Saul, D., Kosinsky, R. L., Atkinson, E. J., Doolittle, M. L., Zhang, X., LeBrasseur, N. K., Pignolo, R. J., Robbins, P. D., Niedernhofer, L. J., Ikeno, Y., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-32552-1 · Cited by 1,060 · see citing works
- Authors
- Florez-Sampedro, L., Soto-Gamez, A., Poelarends, G. J., & Melgert, B. N.
- Affiliations
- Department of Chemical and Pharmaceutical Biology, Groningen Research Institute of Pharmacy, University of Groningen, Groningen, The Netherlands
- University Medical Center Groningen (NL)
- University of Groningen (NL)
- Corresponding author
- Melgert, Barbro N.
- Venue
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Publisher
- American Physiological Society
- Published
- 2020-06-01
- Volume
- 318
- Issue
- 6
- Pages
- L1183-L1197
- ISSN
- 1040-0605 (ISSN-L)
- 1522-1504
- OpenAlex
- W3013790306
- Cited by
- 47
- References
- 108
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 8 · 2023: 7 · 2022: 8 · 2021: 10 · 2020: 2
- FWCI
- 0.66
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal of Physiology-Lung Cellular and Molecular Physiology (publishedVersion)
- PubMed (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion, other-oa)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, other-oa)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Macrophage Migration Inhibitory Factor
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Keywords
- macrophage migration inhibitory factor, chronic lung disease, MIF knockout mice, spontaneous emphysema, growth factors, embryonic development, lung development, inflammation
- MeSH terms
- Animals, Chronic Disease, Humans, Inflammation, Lung Diseases, Macrophage Migration-Inhibitory Factors
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.
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