TMEM173 has been reported to participate in endoplasmic reticulum stress, inflammation and immunology, all of which closely involved with cardiac hypertrophy. But its role in autophagy is not fully figured out. In our research, Tmem173 global knockout (KO) mice manifested more deteriorated hypertrophy, fibrosis, inflammatory infiltration and cardiac malfunction compared with wild type C57BL/6 mice after 6 weeks of transverse aortic constriction. And KO mice showed inhibited autophagosome degradation in myocardium observed under transmission electron microscope and in protein level. In in vitro experiments conducted in neonatal rat cardiomyocytes under phenylephrine treatment, the abundance of Tmem173 gene was negatively related to the abundance of LC3‐Ⅱ and the number of red and yellow fluorescent dots, of which reflected the capacity of autophagosome degradation. These results indicated that TMEM173 might be a promoter of autophagic flux and protected against pressure overload‐induced cardiac hypertrophy. It may serve as a potential therapeutic target for cardiac hypertrophy in the future.

中文翻译：

---

TMEM173 通过调节自噬防止压力超负荷引起的心脏肥大

据报道，TMEM173 参与内质网应激、炎症和免疫学，所有这些都与心脏肥大密切相关。但它在自噬中的作用尚未完全弄清楚。在我们的研究中，与野生型 C57BL/6 小鼠相比，Tmem173全局敲除 (KO) 小鼠在横向主动脉缩窄 6 周后表现出更严重的肥大、纤维化、炎症浸润和心脏功能障碍。并且在透射电子显微镜下和蛋白质水平观察到，KO小鼠在心肌中显示出抑制的自噬体降解。在去氧肾上腺素处理下对新生大鼠心肌细胞进行的体外实验中，Tmem173的丰度基因与LC3-Ⅱ丰度和红黄荧光点数呈负相关，反映自噬体降解能力。这些结果表明 TMEM173 可能是自噬通量的启动子，并防止压力超负荷引起的心脏肥大。它可以作为未来心脏肥大的潜在治疗靶点。