Breakdown of Epithelial Barrier Integrity and Overdrive Activation of Alveolar Epithelial Cells in the Pathogenesis of Acute Respiratory Distress Syndrome and Lung Fibrosis
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Individual alveolar epithelial cells (AECs) collaboratively form a tight barrier between atmosphere and fluid-filled tissue to enable normal gas exchange. The tight junctions of AECs provide intercellular sealing and are integral to the maintenance of the AEC barrier integrity. Disruption and failure of reconstitution of AEC barrier result in catastrophic consequences, leading to alveolar flooding and subsequent devastating fibrotic scarring. Recent evidences reveal that many of the fibrotic lung diseases involve AECs both as a frequent target of injury and as a driver of ongoing pathological processes. Aberrantly activated AECs express most of the growth factors and chemokines responsible for the proliferation, migration, and activation of fibroblasts. Current evidences suggest that AECs may acquire overdrive activation in the initial step of fibrosis by several mechanisms, including abnormal recapitulation of the developmental pathway, defects of the molecules essential for epithelial integrity, and acceleration of aging-related properties. Among these initial triggering events, epithelial Pten, a multiple phosphatase that negatively regulates the PI3K/Akt pathway and is crucial for lung development, is essential for the prevention of alveolar flooding and lung fibrosis through the regulation of AEC barrier integrity after injury. Reestablishment of AEC barrier integrity also involves the deployment of specialized stem/progenitor cells.
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Excessive and persistent damage to alveolar architecture often precedes dysregulated tissue repair processes and fibrosis.
“The observed loss of alveolar basement membrane integrity indicates excessive and persistent damage to the alveolar architecture, which often precedes dysregulated tissue repair processes and fibrosis (16, 17).”
From Lung epithelial and endothelial damage, loss of tissue repair, inhibition of fibrinolysis, and cellular senescence in fatal COVID-19 (2021) · cites this paper as [16]
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- Authors
- Yanagi, S., Tsubouchi, H., Miura, A., Matsumoto, N., & Nakazato, M.
- Affiliations
- University of Miyazaki (JP)
- Corresponding author
- Yanagi, Shigehisa
- Venue
- BioMed Research International
- Publisher
- Wiley
- Published
- 2015
- Volume
- 2015
- Pages
- 1-12
- ISSN
- 1110-7243 (ISSN-L)
- 2314-6133
- 2314-6141
- PMC
- PMC4615219
- OpenAlex
- W2114698744
- Cited by
- 71
- References
- 92
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 8 · 2023: 5 · 2022: 11 · 2021: 8 · 2020: 16 · 2019: 3 · 2018: 7 · 2017: 6 · 2016: 2
- FWCI
- 0.89
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- BioMed Research International (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Japan Society for the Promotion of Science (20790573, 22790763)
- Takeda Science Foundation (20790573, 22790763)
- Japan Intractable Disease Research Foundation (20790573, 22790763)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Neonatal Respiratory Health Research
- Keywords
- acute respiratory distress syndrome, pulmonary fibrosis, alveolar epithelial cells, epithelial barrier integrity, tight junctions, PTEN, PI3K/Akt signaling, alveolar flooding, fibroblast activation, chemokines, stem/progenitor cells, lung development
- MeSH terms
- Aging, Animals, Epithelial Cells, Fibroblasts, Humans, Lung, Pulmonary Alveoli, Pulmonary Fibrosis, Respiratory Distress Syndrome, Stem Cells, Phosphatidylinositol 3-Kinases, Cell Proliferation, PTEN Phosphohydrolase, Mice
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