A narrative review of autophagy in migraine
Abstract
Background and objective: Autophagy is a natural process regulated by autophagy-related genes in eukaryotic cells that involves the degradation of cytoplasmic proteins and old or damaged organelles via the lysosomal pathway to help maintain cell homeostasis. Previous studies have suggested a potential association between autophagy and migraine, while the underlying mechanisms remain unclear. This review seeks to evaluate the possible involvement of autophagy in the pathophysiology of migraine, aiming to clarify its role and implications for future research and therapeutic strategies. Methods: A search in PubMed was conducted for English-language articles until December 5, 2024. Key terms of "autophagy," "migraine," "microglia," "neurogenic inflammation," "central sensitization," "mitophagy" and "neuropathic pain" in different combinations. Results: In the context of migraine, the activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (PKB/Akt) signaling pathway exerts a direct influence on the mammalian target of rapamycin (mTOR), leading to a reduction in autophagy levels. Moreover, the stimulation of purinergic ligand-gated ion channel type 7 receptor (P2X7R) in microglia can hinder autophagy by interfering with the fusion of autophagosomes and lysosomes, which impedes the degradation of substrates within the autophagolysosome. Increased levels of calcitonin gene-related peptide (CGRP) may also modulate autophagy through the Akt/mTOR or protein kinase A…
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