ArticleExperimental animals2023
Carbon monoxide ameliorates lipopolysaccharide-induced acute lung injury via inhibition of alveolar macrophage pyroptosis.
Article in Experimental animals, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Mechanisms and therapeutic strategies of pyroptosis in sepsis‑induced acute lung injury (Review).International journal of molecular medicine · 2026Review
- Progress of alveolar macrophages in biological function and acute lung injury/acute respiratory distress syndrome.Frontiers in immunology · 2025Review
- On the Question of CO's Ability to Induce HO-1 Expression in Cell Culture: A Comparative Study Using Different CO Sources.ACS chemical biology · 2024Article
- Interleukin-6 and pulmonary hypertension: from physiopathology to therapy.Frontiers in immunology · 2023Review
- COVID-19 Mimics Pulmonary Dysfunction in Muscular Dystrophy as a Post-Acute Syndrome in Patients.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carbon monoxide (CO) has been reported to exhibit a therapeutic effect in lipopolysaccharide (LPS)-induced acute lung injury (ALI). However, the precise mechanism by which CO confers protection against ALI remains unclear. Pyroptosis has been recently proposed to play an essential role in the initiation and progression of ALI. Thus, we investigated whether pyroptosis is involved in the protection of CO against ALI and its underlying mechanism. First, an LPS-induced ALI mouse model was established. To determine the role of pyroptosis, we evaluated histological changes and the expression levels of cleaved caspase-11, N-gasdermin D (GSDMD), and IL-1β in lung tissues, which are the indicators of pyroptosis. Inhalation of CO exhibited protective effects on LPS-induced ALI by decreasing TNF-α and IL-10 expression and ameliorating pathological changes in lung tissue. In vitro, CO significantly reduced the expression of cleaved caspase-11, N-GSDMD, IL-1β, and IL-18. In addition, it increased nuclear factor E2-related factor 2 (NRF-2) expression in a time-dependent manner in RAW 264.7 cells and decreased N-GSDMD expression. The expression of cleaved GSDMD and release of LDH were increased after treatment with a specific NRF-2 inhibitor, ML385, indicating that NRF-2 mediates the inhibition of pyroptosis by CO. Taken together, these results demonstrated that CO upregulated NRF-2 to inhibit pyroptosis and subsequently ameliorated LPS-induced ALI.
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Registered trials
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.