ArticleMolecular biology reports2026
Overexpression of miR-7641 activates ox-LDL-induced autophagy in macrophages by regulating USP7.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThe present study aimed to clarify the function of miR-7641 in atherosclerosis (AS) and to elucidate the molecular basis of its modulation of ox-LDL-triggered autophagy in macrophages through Ubiquitin-Specific Protease 7 (USP7).
methodsAn in vitro AS model was generated by exposing human THP-1 macrophages to ox-LDL. Experimental manipulation included transfection with miR-7641 mimics, introduction of a USP7 overexpression plasmid, and administration of the autophagy inhibitor 3-methyladenine (3-MA). Transcript and protein levels were determined by RT-qPCR and Western blot, respectively. Cytokine release was assessed via ELISA. The binding interaction between miR-7641 and USP7 was validated using a dual-luciferase reporter assay.
resultsmiR-7641 levels were markedly elevated in macrophages following ox-LDL stimulation. Forced expression of miR-7641 attenuated the synthesis and secretion of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6. At the mechanistic level, miR-7641 counteracted ox-LDL-mediated inhibition of macrophage autophagy, as indicated by an increased LC3B-II/I ratio, enhanced Beclin-1 expression, and decreased P62 accumulation. Dual-luciferase analysis verified that miR-7641 directly bound to the 3’-UTR of USP7. In contrast, USP7 overexpression reduced autophagic activity and intensified inflammatory signaling. Notably, restoration of USP7 expression partially abolished the autophagy-promoting and inflammation-suppressive effects mediated by miR-7641.
conclusionsmiR-7641 promotes cytoprotective autophagy in macrophages and mitigates ox-LDL-induced inflammatory activation through direct repression of its downstream target USP7. The miR-7641/USP7/autophagy axis represents a newly characterized regulatory circuit in macrophage dysfunction during AS and may offer promising molecular targets for therapeutic intervention.
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