ArticleMolecular medicine reports2020
Inhibition of calcineurin/NFATc4 signaling attenuates ventilator‑induced lung injury.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Mechanotransducer Piezo1 drives ventilator‑induced lung injury in lung epithelial cells via the calcineurin/NFATc3 pathway.Molecular medicine reports · 2026Article
- Matrine alleviates coronary microvascular dysfunction in ischemia with non-obstructive coronary artery disease mice induced by advanced glycation end products inhibition of the reactive oxygen species-mediated endoplasmic reticulum stress in cardiac microvascular endothelial cells.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Article
- Nuclear Factor of Activated T Cells (NFAT) Proteins as Targeted Molecules in Diseases: A Narrative Review.Cureus · 2024Review
- Regulation of cell proliferation and transdifferentiation compensates for ventilator-induced lung injury mediated by NLRP3 inflammasome activation.Immunity, inflammation and disease · 2023Review
- Single cell transcriptomic analysis of murine lung development on hyperoxia-induced damage.Nature communications · 2021Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
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Abstract
Ventilator‑induced lung injury (VILI) is a life‑threatening condition caused by the inappropriate use of mechanical ventilation (MV). However, the precise molecular mechanism inducing the development of VILI remains to be elucidated. In the present study, it was revealed that the calcineurin/NFATc4 signaling pathway mediates the expression of adhesion molecules and proinflammatory cytokines essential for the development of VILI. The present results revealed that a high tidal volume ventilation (HV) caused lung inflammation and edema in the alveolar walls and the infiltration of inflammatory cells. The calcineurin activity and protein expression in the lungs were increased in animals with VILI, and NFATc4 translocated into the nucleus following calcineurin activation. Furthermore, the translocation of NFATc4 and lung injury were prevented by a calcineurin inhibitor (CsA). Thus, the present results highlighted the critical role of the calcineurin/NFATc4 signaling pathway in VILI and suggest that this pathway coincides with the release of ICAM‑1, VCAM‑1, TNF‑α and IL‑1β.
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