This review analyzes the ceRNA network's role in mast cell activation, highlighting regulatory mechanisms and therapeutic implications.
Background Chronic Urticaria (CU) is an inflammatory skin disease driven by aberrant mast cell (MC) activation, yet 30% of patients respond poorly to available therapies. Recent studies have identified the competitive endogenous RNA (ceRNA) network as a key mechanism regulating mast cell signaling, but the specific mechanism of its hierarchical regulation has not been fully elucidated. Objective The aim of this review is to analyze the role of the ceRNA network in maintaining sustained mast cell activation, to propose a three-tiered regulatory model, and to evaluate strategies for its translation to precision therapy. Method Systematic PubMed/Web of Science analysis (2000-2024) using keywords ("chronic urticaria" AND ("ceRNA" OR "lncRNA" OR "circRNA") AND ("mast cell")) integrated ceRNA-pathway mechanisms, with evidence-anchored schematics via GDP. Conclusion The ceRNA network functions through three levels of hierarchical regulation: (1) core RNAs (e.g. NEAT1) adsorb miRNAs to deregulate key signaling pathways; (2) shared miRNAs (e.g. miR-155) connect upstream and downstream targets; and (3) effector molecules (e.g. STAT3) drive mast cell activation. RNA therapeutics or exosome delivery technologies targeting these axes are expected to provide new strategies for refractory CSU.
No takes yet. Share an insight, caveat, or question.
He et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: