ArticleJournal of thoracic disease2024
Sivelestat sodium alleviated sepsis-induced acute lung injury by inhibiting TGF-β/Smad signaling pathways through upregulating microRNA-744-5p.
Article in Journal of thoracic disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- [Natural bear bile powder attenuates lipopolysaccharide-induced acute lung injury in mice by regulating the NF-κB and Nrf-2/HO-1 signaling pathways].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Salvianolic Acid B Upregulates miR-744-5p Expression in Peripheral Blood Mononuclear Cell-Derived Extracellular Vesicles to Alleviate Uremic Cardiomyopathy.Journal of extracellular vesicles · 2026Article
- The relationship between serum levels of miR-342 and miR-148a and acute lung injury in sepsis patients.Open medicine (Warsaw, Poland) · 2026Article
- Sivelestat sodium alleviates sepsis-associated acute lung injury by inhibiting ferroptosis via the Nrf2/SLC7A11/GPX4 axis.PloS one · 2026Article
- Regulation of inflammatory lung injury and repair by transforming growth factors.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Circulating extracellular vesicles as potential biomarkers and mediators of acute respiratory distress syndrome in sepsis.Scientific reports · 2025Article
- Effect of sivelestat on postoperative outcomes in patients with acute type A aortic dissection and hypoxemia: a retrospective analysis.American journal of cardiovascular disease · 2025Article
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Authors and funding
5 authors.
Funding
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Abstract
Background: Acute lung injury (ALI) is one of the most common critical illnesses in clinical practice, with sepsis being the most common cause of ALI. Sivelestat sodium (SV) hydrate is a highly effective inhibitor of neutrophil elastase, specifically targeting ALI related to systemic inflammatory response syndrome. The aim of this study is to examine the mechanisms by which SV can reduce the severity of ALI resulting from sepsis. Methods: Cecum ligation and puncture (CLP) was employed for creating an animal model of ALI caused by sepsis. Primary human pulmonary microvascular endothelial cells (HPMECs) were treated with lipopolysaccharide (LPS) to develop an Results: In both Conclusions: The upregulation of miR-744-5p by SV inhibits the TGF-β/Smad signaling pathway, thereby reducing sepsis-induced ALI.
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