ArticleAmerican journal of respiratory cell and molecular biology2025
Macrophage S1PR2 Drives Sepsis-induced Immunosuppression by Exacerbating Mitochondrial Fragmentation.
Article in American journal of respiratory cell and molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Immunometabolic Reprogramming in Experimental Sepsis: A Driver of Multiple Organ Dysfunction Syndrome.Journal of inflammation research · 2026Review
- Review
- The emerging role of ferroptosis in the pathological development and progression of sepsis.Military Medical Research · 2025Review
- Rethinking post-sepsis syndrome: linking cellular dysfunction to the clinical picture.Critical care (London, England) · 2025Review
- Targeting S1PR2 in Sepsis, One Fragmented Mitochondrion at a Time.American journal of respiratory cell and molecular biology · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
Macrophage mitochondrial dysfunction is associated with immunosuppression and poor prognosis of patients with sepsis. Mitochondrial fragmentation drives mitochondrial dysfunction. Our previous study has found that S1PR2 (sphingosine-1-phosphate receptor 2) regulates macrophage phagocytosis during sepsis, whereas the role of S1PR2 in immunosuppression and the mechanisms require further study. This study aimed to unveil the relationship between macrophage mitochondrial fragmentation and sepsis-induced immunosuppression, as well as the S1PR2-related mechanisms thereof. Peripheral blood monocytes were collected from healthy control subjects (
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