Attenuation of ventilator-induced lung injury through suppressing the pro-inflammatory signaling pathways: A review on preclinical studies

Monjezi, Mojdeh; Jamaati, Hamidreza; Noorbakhsh, Farshid

doi:10.1016/j.molimm.2021.04.007

Cited by 11 publications

(7 citation statements)

References 90 publications

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“…Small tidal volumes and low airway pressures may reduce the morbidity and mortality of VILI [ 5 ]. In addition to canonical inflammation-related molecules including innate immune cytokines and chemokines [ 6 ], the permeability-originating obstruction response in which alveolar leakage leads to surfactant dysfunction and increases local tissue stresses also plays a critical role in VILI [ 7 ]. Thus, it is of great importance to understand the molecular mechanism of VILI and develop new preventive/therapeutic interventions.…”

Section: Introductionmentioning

confidence: 99%

Fibroblast growth factor 21 attenuates ventilator-induced lung injury by inhibiting the NLRP3/caspase-1/GSDMD pyroptotic pathway

et al. 2023

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Background Ventilator-induced lung injury (VILI) is caused by overdistension of the alveoli by the repetitive recruitment and derecruitment of alveolar units. This study aims to investigate the potential role and mechanism of fibroblast growth factor 21 (FGF21), a metabolic regulator secreted by the liver, in VILI development. Methods Serum FGF21 concentrations were determined in patients undergoing mechanical ventilation during general anesthesia and in a mouse VILI model. Lung injury was compared between FGF21-knockout (KO) mice and wild-type (WT) mice. Recombinant FGF21 was administrated in vivo and in vitro to determine its therapeutic effect. Results Serum FGF21 levels in patients and mice with VILI were significantly higher than in those without VILI. Additionally, the increment of serum FGF21 in anesthesia patients was positively correlated with the duration of ventilation. VILI was aggravated in FGF21-KO mice compared with WT mice. Conversely, the administration of FGF21 alleviated VILI in both mouse and cell models. FGF21 reduced Caspase-1 activity, suppressed the mRNA levels of Nlrp3, Asc, Il-1β, Il-18, Hmgb1 and Nf-κb, and decreased the protein levels of NLRP3, ASC, IL-1β, IL-18, HMGB1 and the cleaved form of GSDMD. Conclusions Our findings reveal that endogenous FGF21 signaling is triggered in response to VILI, which protects against VILI by inhibiting the NLRP3/Caspase-1/GSDMD pyroptosis pathway. These results suggest that boosting endogenous FGF21 or the administration of recombinant FGF21 could be promising therapeutic strategies for the treatment of VILI during anesthesia or critical care.

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Section: Introductionmentioning

confidence: 99%

Fibroblast growth factor 21 attenuates ventilator-induced lung injury by inhibiting the NLRP3/caspase-1/GSDMD pyroptotic pathway

et al. 2023

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“…6 Moreover, ventilator-induced lung injury and ECMO can promote inflammatory cytokine release and leading to complex inflammatory cascades. 7,8 Even though acute kidney injury did not develop in this patient, blood purification was administered early to remove inflammatory mediators. Further, ECMO was removed as soon as inflammation and symptoms resolved.…”

Section: Discussionmentioning

confidence: 96%

Successful treatment of near-fatal asthma with ECMO: A case report and literature review

Tian

Han

2023

Int J Artif Organs

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Near-fatal asthma (NFA) can lead to severe hypercapnia and sudden cardiac arrest; however, it can be reversed by extracorporeal membrane oxygenation (ECMO). We report a case of a 37-year-old male diagnosed with NFA. After fluid rehydaration, spasmolysis, and treatment with glucocorticoid and mechanical ventilation, the patient’s condition improved temporarily. However, his condition worsened rapidly, and the patient presented with progressive respiratory distress, a sharp increase in airway pressure, decreased tidal volume, and barotrauma. The patient was treated with venovenous ECMO in the prone position. Five days later, the patient was successfully weaned from ECMO. Hence, ECMO could be used for NFA at the right time to provide adequate gas exchange for patients in order to reduce lung damage and prevent death.

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“…Beyond COVID-19 treatment, the combination of lidocaine and dexamethasone analyzed in our experiments could be an interesting alternative for other pathological conditions that are driven by an exaggerated inflammatory response, such as ventilator-induced lung injury [ 55 , 56 ].…”

Section: Discussionmentioning

confidence: 99%

Lidocaine reinforces the anti-inflammatory action of dexamethasone on myeloid and epithelial cells activated by inflammatory cytokines or SARS-CoV-2 infection

et al. 2023

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Attenuation of ventilator-induced lung injury through suppressing the pro-inflammatory signaling pathways: A review on preclinical studies

Cited by 11 publications

References 90 publications

Fibroblast growth factor 21 attenuates ventilator-induced lung injury by inhibiting the NLRP3/caspase-1/GSDMD pyroptotic pathway

Fibroblast growth factor 21 attenuates ventilator-induced lung injury by inhibiting the NLRP3/caspase-1/GSDMD pyroptotic pathway

Successful treatment of near-fatal asthma with ECMO: A case report and literature review

Lidocaine reinforces the anti-inflammatory action of dexamethasone on myeloid and epithelial cells activated by inflammatory cytokines or SARS-CoV-2 infection

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