Macrophage polarization via exosomal miR-26a-5p regulation

The phrase "Macrophage polarization from M1 to M2 phenotype via exosomal miR‑26a‑5p regulation" describes a **cellular process** rather than a single molecular target. It refers to the shift of macrophages from the pro-inflammatory M1 state to the anti-inflammatory, tissue-repairing M2 state, which is regulated by microRNA‑26a‑5p delivered through exosomes. This process has been shown to play a key role in modulating inflammation and stabilizing plaques in diseases such as atherosclerosis. Specifically, exosomal miR‑26a‑5p can inhibit PTGS2 expression and suppress NF‑κB signaling, thereby promoting the conversion of macrophages toward an M2 phenotype with anti-inflammatory properties[1]. While this pathway is therapeutically relevant and may be targeted indirectly by drugs or interventions aiming to modulate immune responses or treat inflammatory diseases, it does not represent a single canonical drug target such as an enzyme or receptor but rather describes an axis of cellular communication involving multiple molecules (e.g., microRNAs, PTGS2/COX2, NF-kB)[1][2]. **Note:** This entry is not itself a canonical molecular target but instead refers to a regulatory mechanism/process involving several components. For structured data purposes, consider extracting individual targets such as "microRNA 26a–5p," "PTGS2," or "NF-kappa-B" for more precise mapping.

Other names

Macrophage M1 to M2 polarizationExosomal miR-26a-5p-mediated macrophage polarizationmiR-26a-5p-regulated macrophage phenotype switching