ArticleCommunications biology2025
SNX16 aggravates AngII-induced cardiac hypertrophy in mice via EGFR transactivation.
Article in Communications biology, 2025. 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
Cardiac hypertrophy is an independent risk factor for heart failure (HF) which often leads to cardiovascular disease-related death worldwide. Here we show that the upregulated expressions of Sorting Nexin 16 (SNX16) are evident in the hypertrophic hearts. Cardiac-specific deletion of SNX16 significantly inhibited AngII-induced cardiac hypertrophy and cardiomyocytic enlargement in male mice. In addition, we observed that both AngII stimulation and SNX16 overexpression markedly enlarged cardiomyocytes and promoted EGFR transactivation, and these effects were almost completely abolished by AZD9291, an inhibitor of the EGFR pathway. SNX16 deficiency significantly inhibited AngII- or EGF-induced recycling of EGFR in endosomal trafficking in cardiomyocytes. Finally, the elevated expression of SNX16 and the phosphorylation of EGFR and Src were further confirmed in heart tissues from patients with cardiac hypertrophy. Therefore, the present study demonstrates that SNX16-mediated transactivation of EGFR plays a key role in AngII-induced cardiac hypertrophy via enhancing the recycling of EGFR.
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