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In the present study, we sought to identify the role of endoplasmic reticulum stress (ERS) in CTRP9 induced cardioprotection in diabetic heart. Isolated hearts from high\u2010fat\u2010diet (HFD) induced type 2 diabetic Sprague\u2010Dawley rats were subjected to ex vivo IR protocol via a Langendorff apparatus at the presence of globular CTRP9. CTRP9 significantly improved post\u2010IR heart function and reduced cardiac infarction, cardiomyocytes apoptosis, Caspase\u20103, Caspase\u20109, Caspase\u201012, TNF\u2010<jats:italic>\u03b1<\/jats:italic> expression, and lactate dehydrogenase activity. The cardioprotective effect of CTRP9 was associated with reduced ERS and increased expression of disulfide\u2010bond A oxidoreductase\u2010like protein (DsbA\u2010L) in diabetic heart. CTRP9 reduced ERS in thapsigargin (TG) treated cardiomyocytes and protected endoplasmic reticulum (ER) stressed H9c2 cells against simulated ischemia reperfusion (SIR) injury, concurrent with increased expression of DsbA\u2010L. Knockdown of DsbA\u2010L increased ERS and attenuated CTRP9 induced protection against SIR injury in H9c2 cells. Our findings demonstrated for the first time that CTRP9 exerts cardioprotection by reducing ERS in diabetic heart through increasing DsbA\u2010L.<\/jats:p>","DOI":"10.1155\/2016\/1902025","type":"journal-article","created":{"date-parts":[[2016,10,4]],"date-time":"2016-10-04T21:02:30Z","timestamp":1475614950000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["C1q\/TNF\u2010Related Protein 9 Protects Diabetic Rat Heart against Ischemia Reperfusion Injury: Role of Endoplasmic Reticulum 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