ArticleInternational journal of biological sciences2019
Hydrogen sulfide treatment alleviated ventilator-induced lung injury through regulation of autophagy and endoplasmic reticulum stress.
Article in International journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 46 citations in OpenAlex.
- Sulfhydrated TFEB alleviates blast-induced lung injury by maintaining epithelial barrier integrity through the IGF2R/MMP-2/9 pathway.Redox biology · 2026Article
- Hydrogen Sulfide-Regulated NF-κB Signaling via Persulfidation: A Review.Biomolecules · 2026Review
- Mechanical ventilation activates PERK/eIF2α and NOD1 pathways that contribute to NF-κB-driven inflammation in VILI.Respiratory research · 2026Article
- The molecular mechanisms of gas signaling molecules in bronchopulmonary dysplasia related lung injury.Frontiers in cell and developmental biology · 2026Review
- Astaxanthin alleviates autophagy, inflammation, and oxidative stress in ventilator-associated lung injury rats by inhibiting MAPK/ERK1/2 pathway.Acta cirurgica brasileira · 2026Article
- Attenuation of Ventilation-Induced Endoplasmic Reticulum Stress Associated with Lung Injury Through Phosphoinositide 3-Kinase-Gamma in a Murine Endotoxemia Model.International journal of molecular sciences · 2025Article
- Ventilator-induced lung injury in rat models: are they all equal in the race?Laboratory animal research · 2025Review
- mTOR and autophagy in acute lung injury pathogenesis and therapeutic potential.Journal of thoracic disease · 2025Review
- Slow releasing sulphide donor GYY4137 protects mice against ventilator-induced lung injury.Intensive care medicine experimental · 2025Article
- The Role of Hydrogen Sulfide in the Regulation of the Pulmonary Vasculature in Health and Disease.Antioxidants (Basel, Switzerland) · 2025Review
- ASB1 engages with ELOB to facilitate SQOR ubiquitination and HRedox biology · 2025Article
- GYY4137 ameliorates blood brain barrier damage by inhibiting autophagy mediated occludin degradation in cardiac arrest and resuscitation.Scientific reports · 2025Article
- The gut-lung axis in severe pneumonia-related lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Research Hotspots and Frontier Trends of Autophagy in Diabetic Cardiomyopathy From 2014 to 2024: A Bibliometric Analysis.Journal of multidisciplinary healthcare · 2025Article
- Ferritinophagy mediated by the AMPK/ULK1 pathway is involved in ferroptosis subsequent to ventilator-induced lung injury.Respiratory research · 2024Article
- Hydrogen Sulfide: A Versatile Molecule and Therapeutic Target in Health and Diseases.Biomolecules · 2024Review
- Article
- Hydrogen sulfide plays an important role by regulating endoplasmic reticulum stress in myocardial diseases.Frontiers in pharmacology · 2023Review
- Utility of NO and HNitric oxide : biology and chemistry · 2022Review
- Hydrogen Sulfide: A Gaseous Mediator and Its Key Role in Programmed Cell Death, Oxidative Stress, Inflammation and Pulmonary Disease.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanical ventilation has significant therapeutic benefits, but it may cause or aggravate lung injury, which is called ventilator-induced lung injury (VILI). Endogenous hydrogen sulfide (H2S) has roles including regulating inflammation, and promoting vasodilatation; it also exhibits anti-oxidative stress and anti-fibrosis effects. H2S has been reported to alleviate lung injury, but the effects and mechanism of H2S on VILI remain unclear. The present study established a rat model of VILI and treated them with H2S, then measured the changes in respiratory function indicators, lung tissue histopathology, and oxidative, inflammatory, and apoptotic indicators. The effect of H2S on autophagy in the VILI model and the involvement of endoplasmic reticulum (ER) stress were also investigated. To further explore the mechanism, L2 alveolar epithelial cells were treated with cyclic strain to mimic mechanical strain along with the H2S donor NaHS, and the involvement of the NF-κB/MAPK signaling pathway was examined. The results showed that H2S significantly alleviated VILI and inhibited the inflammation and oxidative stress induced by VILI. H2S also significantly reduced autophagy and ER stress in rats. The phosphorylation of IRE1α, PERK and eIF2α and the expression of nuclear ATF4, and GADD34 in L2 cells were all significantly reduced with NaHS. Nuclear NF-κB p65, MAPK p38, JNK, and ERK were all activated by cyclic strain, but inhibited by the ER stress inhibitor 4-PBA or NaHS. Our findings revealed that H2S treatment alleviated VILI by regulating autophagy and ER stress, and the PERK/eIF2α/ATF4/GADD34 and NF-κB/MAPK pathways were involved in the underlying mechanism.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.