The inhibitor of autophagy SBI-0206965 aggravates atherosclerosis through decreasing myeloid-derived suppressor cells
Identifieur interne : 000343 ( Main/Merge ); précédent : 000342; suivant : 000344The inhibitor of autophagy SBI-0206965 aggravates atherosclerosis through decreasing myeloid-derived suppressor cells
Auteurs : Bo Wang [République populaire de Chine] ; Guanjun Dong [République populaire de Chine] ; Qingqiing Zhang [République populaire de Chine] ; Fenglian Yan [République populaire de Chine] ; Zhihua Li [République populaire de Chine] ; Chunxia Li [République populaire de Chine] ; Hui Zhang [République populaire de Chine] ; Qun Ma [République populaire de Chine] ; Jun Dai [République populaire de Chine] ; Chuanping Si [République populaire de Chine] ; Huabao Xiong [États-Unis]Source :
- Experimental and Therapeutic Medicine [ 1792-0981 ] ; 2019.
Abstract
Atherosclerosis (AS) is currently the leading cause of mortality worldwide, with the development of new strategies to prevent the formation and rupture of atherosclerotic plaques being a paramount area of research. Amounting evidence suggests autophagy has an important role in the pathogenesis of AS and may be a potential therapeutic target. In this study, the effect of SBI-0206965(6965), a novel inhibitor of autophagy, was tested on the development of AS in apolipoprotein E deficient (ApoE−/−) mice. Systemic application of 6965 was found to aggravate AS, with increased plaque size and decreased plaque stability in comparison with the control. Of note, it was observed that 6965 decreased the proportion of myeloid-derived suppressor cells (MDSCs). Further investigation demonstrated MDSCs markedly alleviated AS in ApoE−/− mice; while 6965 reduced the viability and promoted apoptosis of MDSCs
Url:
DOI: 10.3892/etm.2019.8317
PubMed: 32010311
PubMed Central: 6966176
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PMC:6966176Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>Atherosclerosis (AS) is currently the leading cause of mortality worldwide, with the development of new strategies to prevent the formation and rupture of atherosclerotic plaques being a paramount area of research. Amounting evidence suggests autophagy has an important role in the pathogenesis of AS and may be a potential therapeutic target. In this study, the effect of SBI-0206965(6965), a novel inhibitor of autophagy, was tested on the development of AS in apolipoprotein E deficient (ApoE<sup>−/−</sup>
) mice. Systemic application of 6965 was found to aggravate AS, with increased plaque size and decreased plaque stability in comparison with the control. Of note, it was observed that 6965 decreased the proportion of myeloid-derived suppressor cells (MDSCs). Further investigation demonstrated MDSCs markedly alleviated AS in ApoE<sup>−/−</sup>
mice; while 6965 reduced the viability and promoted apoptosis of MDSCs <italic>in vitro</italic>
. This is the first study describing an association between autophagy and MDSCs in AS models, providing a novel mechanism to potentially target in the management of this condition.</p>
</div>
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