ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Emodin Alleviates Sepsis-Induced Multiorgan Damage by Inhibiting NETosis through Targeting Neutrophils BCL-10.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- ActivatableChemical science · 2026Article
- Targeting FAR1 to inhibit intestinal macrophage ferroptosis: repurposing irinotecan as a novel sepsis therapy.Apoptosis : an international journal on programmed cell death · 2026Article
- Macrophage Extracellular Traps in Immunity and Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- All-in-one: a CGRP-encapsulated Rh-GelMA supramolecular dual-network hydrogel orchestrating immune-vascular coupling for diabetic wound healing.Journal of nanobiotechnology · 2026Article
- IL-8-driven neutrophil NETosis triggers endothelial apoptosis and exacerbates preeclampsia.Journal of translational medicine · 2026Article
- Dachengqi Decoction: emerging therapeutic potential in sepsis and target organ injury.Frontiers in pharmacology · 2026Review
- In-vivo Antioxidant Effects of Emodin on Ischemia-Reperfusion Injury of Rat's Skeletal Muscle.Drug design, development and therapy · 2026Article
- Platinum-doped emodin carbon dots mitigate sepsis-induced lung injury by targeting the gut-lung axis.Journal of nanobiotechnology · 2025Article
- Emodin Alleviates Sepsis-Induced Multiorgan Damage by Inhibiting NETosis through Targeting Neutrophils BCL-10.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Sepsis is a life-threatening condition caused by dysregulated host responses to infection, characterized by excessive inflammation and abnormal coagulation. Neutrophil extracellular traps (NETs) formation bridges these two pathological processes. Through both in vivo and in vitro experiments, it is observed that Emodin, a natural anthraquinone derivative derived from Dahuang, significantly ameliorates the cytokine storm and coagulation abnormalities induced by sepsis, demonstrating remarkable efficacy in inhibiting NETs formation. Furthermore, through protein microarrays, surface plasmon resonance (SPR), pull-down assays, and molecular docking analyses, BCL-10 is established as a direct target of Emodin, providing protective effects in both in vivo and in vitro settings. Through conditional knockout of BCL-10 in neutrophils, alongside single-cell sequencing analyses, it is confirmed that BCL-10 is key in promoting excessive NET formation in sepsis. Additionally, Emodin exerts powerful protective effects by modulating the function of the BCL-10/MALT1 complex, thereby alleviating the NF-κB signaling activation and inhibiting NETs formation. Collectively, these findings provide pharmacological evidence that Emodin targeted BCL-10 regulates the BCL-10/MALT1 complex and suppresses NF-κB activation, ultimately conferring significant multiorgan protective effects in sepsis. The conduct of this study provides new clues for the translational research of Emodin and its target BCL-10 in sepsis.
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