ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Endothelial-Derived CCL7 Promotes Macrophage Polarization and Aggravates Septic Acute Lung Injury via CCR1-Mediated STAT1 Succinylation.
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 19 papers.
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Who cites it
19 citing papers in PubMed.
- TMEM16F deficiency alleviates sepsis-induced acute lung injury through regulating macrophage polarization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- SIRT7-mediated desuccinylation of FOXO4 suppresses ferroptosis to alleviate LPS-induced acute lung injury.Redox biology · 2026Article
- Review
- GPR132 antagonists alleviate atherosclerosis by suppressing M1 polarization and subsequent VSMCs proliferation and migration as revealed by transcriptomic profiling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Review
- Review
- Deciphering and Targeting the Schwannoma-Neuron-Macrophage Crosstalk for the Treatment of Schwannomatosis and Associated Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Lysine Acetyltransferase 6A Drives M1 Macrophage Polarization Through Metabolic Reprogramming in Sepsis-Induced Acute Lung Injury.Biomolecules · 2026Article
- Hyaluronic acid engineered melanin-MOF nanoreactor synergistically remodeling redox and immune homeostasis for targeted acute lung injury therapy.Materials today. Bio · 2026Article
- The role and therapeutic potential of succinate and succinylation in cardiovascular diseases.Clinical epigenetics · 2026Review
- Succinylation: A novel regulatory axis in cholelithiasis-insights from lysine acetyltransferase 2A/adenosine monophosphate-activated protein kinase signaling.World journal of gastroenterology · 2026Article
- Macrophage metabolic reprogramming in sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2026Review
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Glycolysis-related gene signatures in spinal cord injury pathophysiology identification through integrative gene expression analysis.Frontiers in genetics · 2026Article
- Succinylation: novel molecular mechanisms and prospects for targeted therapy in liver diseases.Frontiers in molecular biosciences · 2026Review
- Mechanisms and therapeutics of immunometabolic reprogramming driving macrophage-ECs interactions in sepsis-associated ARDS from the gut-lung axis perspective.Frontiers in immunology · 2026Review
- Endothelial-Derived CCL7 Promotes Macrophage Polarization and Aggravates Septic Acute Lung Injury via CCR1-Mediated STAT1 Succinylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Anti-inflammatory effects of natural polysaccharides: molecular mechanisms and nanotherapeutic applications.Frontiers in immunology · 2025Review
- From "metabolic storm" to "immune paralysis": the dynamic evolution of macrophages and metabolism reprogramming in ARDS.Frontiers in immunology · 2025Review
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Authors and funding
6 authors.
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Abstract
Acute lung injury (ALI) is a significant complication of sepsis, wherein the interaction between pulmonary vascular endothelial cells and immune cells plays a pivotal role in the pathogenesis. In this study, it is demonstrated that secretion of chemokine C-C motif ligand 7 (CCL7) by endothelial cells (ECs) induces metabolic reprogramming and M1 polarization of C-C motif chemokine receptor 1-positive (CCR1⁺) macrophages. It is noteworthy that mice with specific inhibition of endothelial-derived CCL7 exhibit reduced severity of septic ALI, underscoring the critical role of CCL7 in the progression of sepsis. Mechanistically, activation of the CCL7-CCR1 axis enhances STAT1 succinylation through upregulation of KAT2A expression, leading to increased STAT1 binding to the promoter of glycolytic genes in macrophages. This epigenetic regulation modulates metabolic reprogramming and M1 polarization of macrophages, thereby driving inflammatory cascades in septic ALI. Furthermore, in sepsis models, Ccr1-knockout (Ccr1
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