ArticleCell death and differentiation2026
Macrophage USP7 aggravates acute myocardial infarction by inhibiting STING degradation through the ESCRT pathway.
Article in Cell death and differentiation, 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
Macrophage-driven inflammation plays a critical role in the progression of acute myocardial infarction (AMI). This study revealed that USP7 expression was elevated in peripheral blood mononuclear cells (PBMCs) from patients with coronary artery disease (CAD). Furthermore, in a mouse model of myocardial infarction (MI), after AMI cardiac inflammation was suppressed by macrophage-specific USP7 knockout. Mechanistically, USP7 directly interacted with STING and suppressed its K63-linked ubiquitination at residue K289, thereby preventing STING degradation via the endosomal sorting complex required for transport (ESCRT)-lysosomal pathway and enhancing STING-mediated inflammatory signaling. The cardioprotective effects of USP7 ablation were abrogated by STING overexpression. Moreover, pharmacological inhibition of USP7 or adenovirus-mediated knockdown of USP7 similarly attenuated AMI-induced cardiac injury and inflammation in mice. These findings identify USP7 as a novel deubiquitinating enzyme that regulates STING ubiquitination and degradation via the ESCRT pathway, thus establishing USP7 as a critical regulator of macrophage inflammatory responses in AMI.
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Registered trials
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