Key result
Hyperthermia drives atrial fibrosis via exosomal miR-210-3p and PI3K/AKT activation, an effect suppressed by LY294002.
Why the study?
This study sought to examine the role of atrial myocyte-derived exosomal miR-210-3p in the progression of atrial fibrosis following hyperthermia.
Does hyperthermia-induced exosomal miR-210-3p promote atrial fibrosis via the GPD1L/PI3K/AKT pathway?
Does hyperthermia-induced exosomal miR-210-3p promote atrial fibrosis via the GPD1L/PI3K/AKT pathway?
Hyperthermia upregulates exosomal miR-210-3p, which targets GPD1L to activate the PI3K/AKT pathway and promote atrial fibrosis, offering a potential mechanism for fibrosis after insufficient radiofrequency ablation.
May explain post-ablation fibrosis; hypothesis-generating and requires human validation before targeting.
OBJECTIVE: This study seeks to examine the role of miR-210-3p, delivered by atrial myocyte-derived exosomes, in the progression of atrial fibrosis after hyperthermia. METHODS: highly expressed in myocardial cells. The GSE31821 dataset from the GEO database was further analyzed, revealing significant gene expression differences between atrial fibrillation (AF) patients and sinus rhythm controls, with enrichment analysis identifying key fibrosis-related pathways. Then, an AF cell model was established and exposed to hyperthermia to simulate the effects of insufficient radiofrequency ablation (IRFA). RESULTS: knockdown significantly enhanced the activation of the PI3K/AKT pathway. Additionally, the PI3K/AKT inhibitor LY294002 effectively suppressed pro-fibrotic effects. CONCLUSION: , providing new potential targets and mechanisms for the treatment of AF-related fibrosis.
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Li et al. (2025) studied Atrial fibrillation and atrial fibrosis. Hyperthermia and PI3K/AKT inhibitor LY294002 was evaluated on Activation of the PI3K/AKT pathway and pro-fibrotic effects. Hyperthermia upregulates exosomal miR-210-3p to target GPD1L, activating the PI3K/AKT pathway and promoting atrial fibrosis, which was effectively suppressed by the inhibitor LY294002.
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