Naringin targets JAK1-mediated M2 polarization of macrophages to promote the osteogenic effect of induced membrane technique.

Unraveling the therapeutic mechanisms of Polygonum cuspidatum in pulmonary fibrosis: Modulation of M2 macrophage polarization and glycolysis pathways.

Kaempferol reprograms pro-inflammatory macrophage polarization by targeting the PTGS2-PGE2 axis: A multi-omics deconvolution of a traditional anti-inflammatory herb pair.

Glucose modulates macrophage polarization via glycating adsorbed albumin on titanium.

Vitamin D receptor drives macrophage M2 polarization and exacerbates airway inflammation in asthma.

Isoeugenol suppression of osteoporosis by modulating macrophage M1 Polarization via p38 MAPK and arachidonic acid metabolism pathways.

Lung cancer cell-derived exosomal EHF drives M2 macrophage polarization via transcriptional activation of RNF41 to promote tumor progression

PZP deficiency impairs M2 macrophage polarization via TGF-β/Smad3 signaling, contributing to immune dysregulation at the maternal-fetal interface in preeclampsia.

Targeting SERPINE1 enhances PD-1 blockade response by modulating macrophage infiltration and polarization through the STAT3-CCL2 axis in non-small cell lung cancer.

Liraglutide prevents lupus-associated diffuse alveolar hemorrhage via inhibiting lymphocyte infiltration and promoting macrophage M2 polarization.

Electroacupuncture at PC6 mediates cardioprotection by vagal afferent-sympathetic efferent anti-inflammatory pathway in myocardial infarction mouse.

Acute to chronic liver macrophage response in Syrian hamsters infected with the liver fluke Opisthorchis felineus.

Lpar3-mediated macrophage polarization promotes inflammatory tooth extraction socket healing and alveolar bone regeneration.

Quercetin-driven M2 polarization of macrophages via ALOX5 inhibition in kupffer cells: A strategy for mouse liver fibrosis treatment.

Mycobacterium tuberculosis escapes immunity by regulating FUS/TLR4 and metabolic reprogramming to suppress macrophage activity

Integrated whole transcriptome sequencing, network pharmacology and in vivo validation reveal that Compound Wufengcao Liquid promotes pressure injury healing via PPARγ-mediated macrophage polarization.

Ailanthone ameliorates CCl4-induced liver fibrosis by targeting PKM2-mediated macrophage M1 polarization and glycolytic reprogramming.

Supramolecularly co-assembled composite bone cement prepared from tea polyphenol-modified tricalcium phosphate/tricalcium silicate with osteogenic, antibacterial, and immunomodulatory effects.

Ultrasound-guided HUC-MSCs transplantation alleviates neuropathic pain in CCI rats: a mechanistic study based on microglia/macrophage polarization and the NLRP3 inflammasome.

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Despite advances in critical care, it remains a major global health challenge, highlighting the urgent need for novel therapeutic approaches. Elevated plasma cell-free DNA (cfDNA) has emerged as a critical driver of inflammation and tissue injury in sepsis. To neutralize its detrimental effects, DNase I can enzymatically degrade circulating cfDNA; however, the clinical application of native DNase I is limited by its rapid degradation and short circulation half-life. Here, we developed a bioengineered delivery system by encapsulating DNase I within M2 macrophage-derived extracellular vesicles (M2-EVs@DNase I), which possess intrinsic targeting ability, high biocompatibility, and low immunogenicity. In a cecal ligation and puncture (CLP)-induced sepsis model, administration of M2-EVs@DNase I significantly reduced circulating cfDNA levels by approximately 60% and suppressed TLR9 activation by about 49%. These effects were accompanied by a shift in macrophage polarization toward an anti-inflammatory M2 phenotype, reduced neutrophil activation, and significant attenuation of lung and kidney injury. Furthermore, treatment with M2-EVs@DNase I significantly improved biochemical indicators of organ function, including ALT, AST, UREA, and CRE levels. Together, these findings demonstrate that M2-EVs@DNase I effectively degrades pathogenic cfDNA and mitigates inflammatory responses, thereby protecting against sepsis-induced multi-organ injury. This study highlights the pathogenic significance of cfDNA in sepsis and introduces M2-EVs@DNase I as a promising biomimetic nanotherapeutic platform for sepsis treatment.