ArticleCell communication and signaling : CCS2020
Phospho-Tyr705 of STAT3 is a therapeutic target for sepsis through regulating inflammation and coagulation.
Article in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 65 citations in OpenAlex.
- Aberrant STAT signaling and T cell dysregulation define a targetable pediatric sepsis endotype.The Journal of clinical investigation · 2026Article
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- A druggable redox switch on SHP1 controls macrophage inflammation.Nature chemical biology · 2026Article
- Secretory LGALS3BP exacerbates sepsis-associated liver dysfunction by activating inflammasome-mediated pyroptosis.Cell death discovery · 2026Article
- A druggable redox switch on SHP1 controls macrophage inflammation.bioRxiv : the preprint server for biology · 2026Article
- Liraglutide alleviates sepsis-associated encephalopathy via attenuating neuronal damage, glial cell activation and mitochondrial dysfunction in a mouse model of sepsis.European journal of medical research · 2026Article
- IFI27-mediated regulation of regulatory T cells aggravates lung injury in sepsis via IL-10/STAT3 signaling.Frontiers in immunology · 2026Article
- Safflower Polysaccharides Alleviate TNBS-Induced Colitis by Modulating Gut Immunity.Foods (Basel, Switzerland) · 2025Article
- Titanium implant can promote M2 polarization with macrophages activation which contribute to osteogenesis and angiogenesis via inactivates JAKS signaling pathway.BMC immunology · 2025Article
- Multifunctional Co-Delivery Systems with Downregulation of the Novel Target PIM1 in Macrophages to Ameliorate TF-Mediated Coagulopathy in Sepsis.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Targeting the STAT3/IL-36G signaling pathway can be a promising approach to treat rosacea.Journal of advanced research · 2025Article
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- Protective effect and mechanism of Sufentanil on acute lung injury in septic mice.Frontiers in pharmacology · 2024Article
- Unphysiological lung strain promotes ventilation-induced lung injury via activation of the PECAM-1/Src/STAT3 signaling pathway.Frontiers in pharmacology · 2024Article
- Evaluation of the ability of commercial enzyme-linked immunosorbent assays to measure mouse tissue factor.Research and practice in thrombosis and haemostasis · 2024Article
- Deficiency of S100A8/A9 attenuates pulmonary microvascular leakage in septic mice.Respiratory research · 2023Article
- STAT3 Signalling Drives LDH Up-Regulation and Adiponectin Down-Regulation in Cachectic Adipocytes.International journal of molecular sciences · 2023Article
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- PD-L1 promotes GSDMD-mediated NET release by maintaining the transcriptional activity of Stat3 in sepsis-associated encephalopathy.International journal of biological sciences · 2023Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSepsis is an infection-induced aggressive and life-threatening organ dysfunction with high morbidity and mortality worldwide. Infection-associated inflammation and coagulation promote the progression of adverse outcomes in sepsis. Here, we report that phospho-Tyr705 of STAT3 (pY-STAT3), not total STAT3, contributes to systemic inflammation and coagulopathy in sepsis.
methodsCecal ligation and puncture (CLP)-induced septic mice were treated with BP-1-102, Napabucasin, or vehicle control respectively and then assessed for systemic inflammation, coagulation response, lung function and survival. Human pulmonary microvascular endothelial cells (HPMECs) and Raw264.7 cells were exposed to lipopolysaccharide (LPS) with pharmacological or genetic inhibition of pY-STAT3. Cells were assessed for inflammatory and coagulant factor expression, cell function and signaling.
resultsPharmacological inhibition of pY-STAT3 expression by BP-1-102 reduced the proinflammatory factors, suppressed coagulation activation, attenuated lung injury, alleviated vascular leakage and improved the survival rate in septic mice. Pharmacological or genetic inhibition of pY-STAT3 diminished LPS-induced cytokine production in macrophages and protected pulmonary endothelial cells via the IL-6/JAK2/STAT3, NF-κB and MAPK signaling pathways. Moreover, the increase in procoagulant indicators induced by sepsis such as tissue factor (TF), the thrombin-antithrombin complex (TAT) and D-Dimer were down-regulated by pY-STAT3 inhibition.
conclusionsOur results revealed a therapeutic role of pY-STAT3 in modulating the inflammatory response and defective coagulation during sepsis. Video Abstract.
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