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This study revealed that RIP<\/jats:styled-content>140 repressed Sirtuin 3 (SIRT<\/jats:styled-content>3), a mitochondrial deacetylase that plays an important role in regulating cardiac function.<\/jats:p><\/jats:sec>Methods<\/jats:title>RIP<\/jats:styled-content>140 was overexpressed by adenovirus infection or was knocked down by RNA<\/jats:styled-content> interference in neonatal rat cardiomyocytes.<\/jats:p><\/jats:sec>Results<\/jats:title>RIP<\/jats:styled-content>140 overexpression repressed, while RIP<\/jats:styled-content>140 silencing elevated the expression and activity of SIRT<\/jats:styled-content>3. Ad\u2010RIP<\/jats:styled-content>140 enhanced the expressions of the cardiac hypertrophic markers and increased cardiomyocyte surface area, whereas SIRT<\/jats:styled-content>3 overexpression prevented the effect of Ad\u2010RIP<\/jats:styled-content>140. Additionally, SIRT<\/jats:styled-content>3 overexpression reversed Ad\u2010RIP<\/jats:styled-content>140\u2010induced mitochondrial dysfunction and energy metabolic dysfunction, such as increase in oxidative stress, decrease in mitochondrial membrane potential and ATP<\/jats:styled-content> production, as well as downregulation of mitochondrial DNA<\/jats:styled-content>\u2010encoded genes and genes related to mitochondrial genome replication and transcription, mitochondrial oxidative phosphorylation and fatty acid oxidation. In contrast, SIRT<\/jats:styled-content>3 silencing exacerbated RIP<\/jats:styled-content>140\u2010induced cardiomyocyte hypertrophy and mitochondrial dysfunction. Furthermore, the repression of SIRT<\/jats:styled-content>3 by RIP<\/jats:styled-content>140 was dependent on estrogen\u2010related receptor\u2010\u03b1 (ERR<\/jats:styled-content>\u03b1). The involvement of peroxisome proliferator\u2010activated receptor\u2010\u03b3 coactivator\u20101\u03b1 (PGC<\/jats:styled-content>\u20101\u03b1) was ruled out of SIRT<\/jats:styled-content>3 suppression by RIP<\/jats:styled-content>140. RIP<\/jats:styled-content>140 and PGC<\/jats:styled-content>\u20101\u03b1 might act as functional antagonists on the regulation of SIRT<\/jats:styled-content>3.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>This study indicates that suppression of SIRT<\/jats:styled-content>3 by RIP<\/jats:styled-content>140 facilitates the development of cardiomyocyte hypertrophy, mitochondrial dysfunction and energy metabolic dysfunction. Strategies targeting inhibition of RIP<\/jats:styled-content>140 and upregulation of SIRT<\/jats:styled-content>3 might improve cardiac energy metabolism and suggest therapeutic potential for heart diseases.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.12800","type":"journal-article","created":{"date-parts":[[2016,9,10]],"date-time":"2016-09-10T13:23:28Z","timestamp":1473513808000},"page":"58-71","source":"Crossref","is-referenced-by-count":22,"title":["Receptor\u2010interacting Protein 140 represses Sirtuin 3 to facilitate hypertrophy, mitochondrial dysfunction and energy metabolic dysfunction in cardiomyocytes"],"prefix":"10.1111","volume":"220","author":[{"given":"J.","family":"You","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology National and Local United Engineering Lab of Druggability and New Drugs Evaluation School of Pharmaceutical Sciences Sun Yat\u2010Sen University Guangzhou 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