ArticleMolecular medicine reports2016
Activation of TRPV1-dependent calcium oscillation exacerbates seawater inhalation-induced acute lung injury.
Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Emerging roles of mechanosensitive ion channels in ventilator induced lung injury: a systematic review.Frontiers in immunology · 2024Pooled it
- Research progress of mitochondrial dysfunction induced pyroptosis in acute lung injury.Respiratory research · 2024Review
- A novel transient receptor potential C3/C6 selective activator induces the cellular uptake of antisense oligonucleotides.Nucleic acids research · 2024Article
- Protective Effect of Vitamin K2 (MK-7) on Acute Lung Injury Induced by Lipopolysaccharide in Mice.Current issues in molecular biology · 2024Article
- Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS).Respiratory research · 2024Review
- The role of TRPV1 in RA pathogenesis: worthy of attention.Frontiers in immunology · 2023Review
- The Effectiveness of Wogonin on Treating Cough Mice With Mycoplasma Pneumoniae Infection.Frontiers in molecular biosciences · 2022Article
- Friend or Foe? The Roles of Antioxidants in Acute Lung Injury.Antioxidants (Basel, Switzerland) · 2021Review
- The potential role of TRPV1 in pulmonary hypertension: Angel or demon?Channels (Austin, Tex.) · 2019Review
- Conjugated polymers optically regulate the fate of endothelial colony-forming cells.Science advances · 2019Article
- NFAT5 participates in seawater inhalation‑induced acute lung injury via modulation of NF-κB activity.Molecular medicine reports · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium is an important second messenger and it is widely recognized that acute lung injury (ALI) is often caused by oscillations of cytosolic free Ca2+. Previous studies have indicated that the activation of transient receptor potential‑vanilloid (TRPV) channels and subsequent Ca2+ entry initiates an acute calcium‑dependent permeability increase during ALI. However, whether seawater exposure induces such an effect through the activation of TRPV channels remains unknown. In the current study, the effect of calcium, a component of seawater, on the inflammatory reactions that occur during seawater drowning‑induced ALI, was examined. The results demonstrated that a high concentration of calcium ions in seawater increased lung tissue myeloperoxidase activity and the secretion of inflammatory mediators, such as tumor necrosis factor‑α (TNF‑α) and interleukin (IL)‑1β and IL‑6. Further study demonstrated that the seawater challenge elevated cytosolic Ca2+ concentration, indicated by [Ca2+]c, by inducing calcium influx from the extracellular medium via TRPV1 channels. The elevated [Ca2+c] may have resulted in the increased release of TNF‑α and IL‑1β via increased phosphorylation of nuclear factor‑κB (NF‑κB). It was concluded that a high concentration of calcium in seawater exacerbated lung injury, and TRPV1 channels were notable mediators of the calcium increase initiated by the seawater challenge. Calcium influx through TRPV1 may have led to greater phosphorylation of NF‑κB and increased release of TNF‑α and IL‑1β.
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