Macrophages are pivotal immune cells that dynamically shift between pro-inflammatory (M1) and anti-inflammatory (M2) activation states, playing dual roles in host defense and tissue homeostasis. Their functional plasticity is tightly regulated by post-transcriptional mechanisms, particularly through RNA-binding proteins (RBPs) that control mRNA stability, translation, and splicing. Emerging evidence suggests that RBPs not only fine-tune macrophage polarization but also critically regulate their survival and death decisions—a balance essential for resolving inflammation or preventing immunopathology. However, the integrated mechanisms by which RBPs coordinate macrophage activation with cell fate choices (apoptosis, pyroptosis, or survival) remain poorly understood.
This Research Topic aims to decipher how specific RBPs differentially regulate macrophage survival and death pathways during activation. It seeks to elucidate the crosstalk between RBP-mediated post-transcriptional control and metabolic reprogramming in polarized macrophages, and to validate the therapeutic potential of targeting RBPs to modulate macrophage-driven inflammation in disease models.
This topic welcomes the following research directions: • The mechanism of RNA-binding proteins in the polarization of macrophages. • The regulation of macrophage survival and death by RBPs. • The regulation of macrophage metabolic reprogramming by RBPs. • The functions of RBPs in macrophage-related diseases. • The potential of RBPs as therapeutic targets for immunotherapy.
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