Aloe vera polysaccharides facilitate diabetic wound healing by promoting macrophage M2 polarization through inhibition of NLRP3 inflammasome activation.

Geometry-driven immunomodulation in 3D-printed bioceramics: Negative curvature promotes macrophage M2 polarization via Ras-MAPK/HIF-1α signaling for vascularized osteogenesis.

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

A chitosan-tea polyphenol composite hydrogel with integrated antibacterial, antioxidant and immunomodulatory functions for the tissue regeneration of MRSA-infected wounds.

A fluorescent hydrogen sulfide donor featuring hydroxyl radical responsiveness promotes diabetic wound healing through the regulation of macrophage polarization.

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

Stage-matched conductive hydrogel with pH/ROS/MMP9 triple-responsive salidroside release for post-infarction myocardial repair.

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

Mesenchymal stem cell‑derived extracellular vesicles (MSC‑EVs) have garnered research attention due to their unique biological functionalities and therapeutic potential. Compared with the parent MSCs from which they originate, MSC‑EVs are typically free from systemic allergic reactions, hemolysis, pyrogenic reactions, abnormal hematological changes, and vascular and muscle irritation problems, and thus, exhibit therapeutic potential. The present review provides a comprehensive analysis of numerous isolation methodologies for MSC‑EVs, with each method being evaluated based on key parameters, including principles, advantages, limitations and applications. Notably, the therapeutic potential of MSC‑EVs in the treatment of tuberculosis (TB) has been emphasized. MSC‑EVs have demonstrated unique capacities to modulate the T helper cell (Th)1/Th2/T regulatory cell balance, promote M2 macrophage polarization, alleviate inflammation through microRNA‑mediated mechanisms and enhance host defense through antimicrobial peptide responses. The integration of MSC‑EVs with anti‑TB therapy can improve lung, kidney and bladder health by reducing TNF‑α levels and increasing IL‑10/TGF‑β ratios. Notably, functional discrepancies between EVs derived from distinct MSC sources, such as umbilical cord vs. bone marrow cells, underscore the need for targeted optimization strategies. Adequate risk assessment is important before clinical trials, particularly concerning immunogenicity, potential pro‑inflammatory effects and promotion of TB latency. The present review explores the potential clinical applications of MSC‑EVs in TB and other infectious diseases, offering key insights into their therapeutic potential, with the aim of guiding future research.

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

Network pharmacology-guided self-assembling quercetin hydrogel from Astragalus membranaceous accelerates diabetic wound healing.

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

A suture-free, microenvironment-adaptive hydrogel actively orchestrating inflammation-to-regeneration transition for abdominal wall defect repair.

MT2A-Mediated Regulation of Cuproptosis in Human Dental Pulp Cells Modulates Macrophage M1 Polarization in Pulpitis.

ACOT8-mediated palmitate accumulation promotes M1 macrophage polarization in renal ischemia-reperfusion injury via activation of the cGAS-STING pathway.

TRIM56 inhibits M1 macrophage polarization and mitigates sepsis-induced acute lung injury via promoting STING ubiquitination-degradation.

The signaling lymphocytic activation molecule family member 8 (SLAMF8) is predominantly expressed on the surface of macrophages and participates in modulating tumor immune microenvironment. However, the role of SLAMF8 in tumor-associated macrophages (TAMs) in gastric cancer (GC) remains unclear. SLAMF8 expression and its association with patient prognosis were analyzed using various online databases. CCK-8 and EdU assays were used to assess GC cell proliferation. A xenograft tumor model was used to assess the in vivo functional role of SLAMF8. SLAMF8 expression was markedly increased and correlated with an unfavorable prognosis in GC. Additionally, SLAMF8 was primarily expressed in macrophages in GC tissues and increased in in vitro-generated-TAMs. SLAMF8 knockdown suppressed M2 polarization, whereas SLAMF8 overexpression promoted M2 polarization in in vitro-generated TAMs. SLAMF8 facilitates TAM-like polarization by coordinately inhibiting NF-κB activation and activating the JAK2/STAT3 signaling pathway. Furthermore, SLAMF8-overexpressing TAMs enhanced the growth of MKN-45 cells both in vitro and in vivo and impaired CD8 + T cell function. SLAMF8 promotes macrophage M2 polarization and accelerates CD8 + T cell dysfunction, thereby facilitating the progression of GC.

Cisplatin (CDDP) resistance remains a formidable obstacle in breast cancer treatment. To address this challenge, we engineered a neutrophil-mediated co-delivery system loaded with a Pt(IV) prodrug (Pt-HPBA) and quercetin (QC). A pH/glutathione (GSH)-dual-responsive nanodrug (Pt-HE@QC/NPs) was constructed via co-assembly of Pt-HPBA and QC. The resulting nanodrugs exhibited high drug loading capacity, maintained excellent colloidal stability under physiological conditions, and rapidly disassembled within the tumor microenvironment, enabling controlled drug release. These nanodrugs were then internalized by neutrophils to form a bio-hybrid delivery system (Pt-HE@QC/NEs). In vitro, Pt-HE@QC/NPs enhanced cellular uptake and exhibited potent cytotoxicity against cisplatin-resistant 4T1/DDP cells. The nanodrug reversed chemoresistance through multiple synergistic mechanisms: inducing mitochondrial dysfunction and reducing intracellular ATP levels to suppress efflux transporter activity; depleting GSH via phenylboronate ester cleavage and Pt(IV) reduction to amplify oxidative stress; and inhibiting GST-π and GPX4 activities to potentiate platinum-induced nuclear toxicity. In vivo, Pt-HE@QC/NEs demonstrated superior tumor-targeting capability and achieved remarkable tumor growth inhibition (TGI: 88.7%). Moreover, this treatment alleviated immunosuppression by triggering immunogenic cell death, enhancing CD8+ T cell infiltration, promoting M1 macrophage polarization, and elevating pro-inflammatory cytokine levels. Notably, systemic toxicity was significantly reduced compared to free CDDP. Collectively, this neutrophil-driven, dual-responsive nanoplatform represents a promising strategy for overcoming cisplatin resistance in breast cancer.

Tumor cell-derived exosomal E2F7 promotes colorectal cancer progression by interacting with SMC4 and induced macrophage M2 polarization.

Cancer therapy is often constrained by targeting single pathogenic mechanisms without addressing the complex tumor microenvironment (TME). Here, we introduce FINAL (Fucoidan-docetaxel Immunomodulatory Nanoparticles as an Antitumoral Lancer), a surface-engineered nanoplatform that simultaneously targets P-selectin-expressing cancer cells and tumor-associated macrophages (TAMs). Beyond targeting specificity, fucoidan surface modification provides intrinsic bioactivities that individually modulate both cell types while coordinately reshaping the TME. FINAL achieves dual-cell orchestration through P-selectin-mediated targeting, activating both receptor-dependent signaling pathways and receptor-independent bioactivities of fucoidan and DTX. P-selectin-mediated targeting enhances cellular uptake and disrupts tumor-TAM adhesion, reducing the level of circulating hybrid cell (CHC) formation. Independent of targeting, fucoidan's bioactivity reduces cellular reactive oxygen species in cancer cells, promotes M1 macrophage polarization, and suppresses VEGF-A-mediated angiogenesis. RNA-seq transcriptomic profiling demonstrated that FINAL drives synergistic immune activation pathways while simultaneously repressing tumor progression signatures, providing mechanistic evidence for concurrent tumor-immune dynamics at the molecular level. In triple-negative breast cancer (TNBC) models, this system-level approach achieved breakthrough therapeutic outcomes, including doubling survival duration, suppressing primary tumor growth, inhibiting lung metastasis, and preserving bone marrow hematopoietic function, demonstrating translational potential compared to conventional docetaxel formulations. Importantly, FINAL maintained therapeutic benefits while reducing systemic toxicity, establishing an optimal balance between antitumor efficacy and safety. The rationally designed fucoidan nanobio interface establishes FINAL as a versatile platform for P-selectin-expressing diseases for next-generation immunochemotherapy agents with broad translational potential across multiple cancer types.