ArticleMedical microbiology and immunology2023
Histone methyltransferase SETD2 inhibits M1 macrophage polarization and glycolysis by suppressing HIF-1α in sepsis-induced acute lung injury.
Article in Medical microbiology and immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 25 citations in OpenAlex.
- Knockdown of PTEN Inhibits Autophagy-Dependent Ferroptosis to Alleviate LPS-Induced Sepsis-Associated Acute Kidney Injury.Inflammation · 2026Article
- Macrophage autophagy-dependent M2 polarization mediates the protective effect of ADSC-conditioned medium against acute lung injury.Stem cell research & therapy · 2026Article
- Essential genetic mutations impair DNA damage repair and modulate tumor immune microenvironment in ccRCC.MedScience · 2026Review
- Exosomes derived from bone marrow mesenchymal stem cells alleviate sepsis-induced ARDS via inhibition of HOXA9-mediated glycolysis in alveolar macrophages.Respiratory research · 2026Article
- Macrophage polarization in hematologic cancers: mechanisms and therapeutic strategies.Blood research · 2026Review
- Interaction networks of macrophage glycolysis and inflammation in sepsis: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Qingzhu granule mitigates acute gouty arthritis through HIF-1α-dependent glycolytic metabolic reprogramming of M1 macrophages.Frontiers in immunology · 2026Article
- Macrophage Hypoxia Signaling Pathways and Their Roles in Sepsis.Journal of inflammation research · 2026Review
- HIF-1α-centered metabolic reprogramming in osteoarthritis: cell type-specific effects and intercellular crosstalk among chondrocytes, BMSCs, and macrophages.Frontiers in immunology · 2026Review
- Clinical immunology in chromatinopathies: a scoping review.Frontiers in immunology · 2026Article
- The Role of Histone Modifications in Acute Lung Injury: Molecular Mechanisms and Potential of Traditional Chinese Medicine Treatment.Journal of inflammation research · 2026Review
- Immunometabolic Reprogramming in Experimental Sepsis: A Driver of Multiple Organ Dysfunction Syndrome.Journal of inflammation research · 2026Review
- Hypoxic microenvironment and pulmonary hypertension.Respiratory research · 2025Review
- Comparative Transcriptomic Analysis Underlies the Differential Virulence ofInternational journal of molecular sciences · 2025Article
- Exploring the effect and mechanism of baicalin on sepsis-induced acute lung injury based on network pharmacology and experimental verification.Scientific reports · 2025Article
- Emerging role of SETD2 in the development and function of immune cells.Genes & diseases · 2025Review
- The role of natural products targeting macrophage polarization in sepsis-induced lung injury.Chinese medicine · 2025Review
- Exploring the Molecular Mechanism by which Kaempferol Attenuates Sepsis-related Acute Respiratory Distress Syndrome Based on Network Pharmacology and Experimental Verification.Current computer-aided drug design · 2025Article
- The fall of the genome protectors triad: PBRM1, SETD2, and BAP1's impact on metabolism and immunity in clear cell renal cell carcinoma.Frontiers in cell and developmental biology · 2025Review
- Decoding the HIF-1-driven metabolic-inflammatory-immune axis in sepsis-associated lung injury: a comprehensive overview.Frontiers in immunology · 2025Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Sepsis is a severe syndrome caused by the imbalance of the host response to infection, accompanied by multiple organ damage, especially acute lung injury. SET Domain-Containing 2 (SETD2) is a methyltransferase catalyzing H3 lysine 36 trimethylation (H3K36me3) that regulates multiple biological processes. This study focused on explicating the action of SETD2 on macrophage function in sepsis and the precise mechanism involved. Enzyme-linked immunosorbent assay, real-time quantitative polymerase chain reaction (RT-qPCR), and Western blotting were used to determine expression. Luciferase reporter assay and chromatin immunoprecipitation assay were conducted to detect the binding of SETD2 or H3K36me3 with the hypoxia-inducible factor 1, alpha subunit (Hif1a) gene. A sepsis-induced acute lung injury model was constructed via cecal ligation and puncture (CLP). SETD2 was decreased in RAW 264.7 cells stimulated by lipopolysaccharide (LPS). Besides, SETD2 suppressed M1 macrophage polarization and glycolysis caused by LPS. HIF-1α was enhanced in RAW 264.7 cells stimulated by LPS and inversely related to SETD2 expression. In addition, SETD2-catalyzed H3K36me3 bound to the Hif1a gene to modulate HIF-1α expression. Furthermore, Hif1a silencing suppressed Setd2 silencing-induced M1 macrophage polarization and glycolysis in RAW 264.7 cells. Moreover, overexpression of Setd2 inhibited CLP-induced lung injury and M1 macrophage polarization in mice. SETD2 suppressed M1 macrophage polarization and glycolysis via regulating HIF-1α through catalyzing H3K36me3 in sepsis.
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