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Autophagy is acknowledged to be an important mechanism regulating cardiac hypertrophy. Sestrin 1, a downstream target gene of p53, has been proven to regulate autophagy. However, the role of Sestrin 1 in cardiac hypertrophy remains unknown. Our study showed that Sestrin 1 <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and protein expression declined in pressure overload cardiac hypertrophy and phenylephrine (<jats:styled-content style=\"fixed-case\">PE<\/jats:styled-content>)\u2010induced cardiac hypertrophy. Knockdown of Sestrin 1 by <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>i deteriorated <jats:styled-content style=\"fixed-case\">PE<\/jats:styled-content>\u2010induced cardiac hypertrophy, whereas the overexpression of Sestrin 1 by adenovirus transfection blunted hypertrophy. We discovered that knockdown of Sestrin 1 resulted in impaired autophagy while overexpression of Sestrin 1 resulted in increased autophagy without affecting lysosomal function. In addition, the antihypertrophic effect of Sestrin 1 overexpression was eliminated by autophagy blockade. Importantly, Sestrin 1 targets at the <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">mTORC<\/jats:styled-content>1\/autophagy pathway to inhibit cardiac hypertrophy by interaction with <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> which is responsible for autophagy regulation. Taken together, our data indicate that Sestrin 1 regulates <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">mTORC<\/jats:styled-content>1\/autophagy axis to attenuate cardiac hypertrophy.<\/jats:p>","DOI":"10.1111\/jcmm.13052","type":"journal-article","created":{"date-parts":[[2017,2,9]],"date-time":"2017-02-09T07:36:51Z","timestamp":1486625811000},"page":"1193-1205","source":"Crossref","is-referenced-by-count":48,"title":["Sestrin 1 ameliorates cardiac hypertrophy <i>via<\/i> autophagy activation"],"prefix":"10.1111","volume":"21","author":[{"given":"Ruicong","family":"Xue","sequence":"first","affiliation":[{"name":"Department of Cardiology The First Affiliated Hospital of Sun Yat\u2010Sen University Guangzhou China"},{"name":"Key Laboratory on Assisted Circulation Ministry of Health Guangzhou 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