心肌肥大
肌球蛋白
免疫球蛋白轻链
肌球蛋白轻链激酶
肌肉肥大
内科学
心脏病学
MYH7
医学
细胞生物学
神经科学
生物
免疫学
抗体
作者
Wenjing Wang,Lili Chen,Yiheng Zhao,Shuchen Zhang,Xiang Zhou
出处
期刊:Research
[American Association for the Advancement of Science]
日期:2025-01-01
卷期号:8
标识
DOI:10.34133/research.0626
摘要
Circular RNAs (circRNAs) are differentially expressed in cardiac hypertrophy; however, the exact function and mechanisms during hypertrophy development are still unknown. Here, we explored the role of a newly discovered circRNA in the pathogenesis of myocardial hypertrophy. It was found that circ-0001283 promoted the progression of cardiac hypertrophy by interacting with myosin light chain 3 (MYL3) to inhibit the protein ubiquitination and enhance its protein expression, not by the competitive endogenous RNA mechanism. Further investigation demonstrated that the reduced hypertrophy induced by circ-0001283 knockdown was counteracted by overexpression of MYL3. Mechanistically, MYL3 facilitated myocardial hypertrophy by inducing autophagy in cells via PI3K/Akt/mTOR and ERK signaling pathways. In summary, circ-0001283 can bind directly to MYL3 and up-regulate its expression, thereby promoting autophagy to accelerate cardiac hypertrophy. Circ-0001283 may serve as a potential therapeutic target for cardiac hypertrophy.
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