Biomed Pharmacother
2019 Oct:118:109407.
doi: 10.1016/j.biopha.2019.109407. Epub 2019 Sep 2.
Preconditioning with endoplasmic reticulum stress alleviated heart ischemia/reperfusion injury via modulating IRE1/ATF6/RACK1/PERK and PGC-1α in diabetes mellitus
Bing Yan 1, Suhuan Liu 1, Xuejun Li 1, Yali Zhong 2, Fei Tong 3, Shuyu Yang 4
Affiliations expand
PMID: 31545290
DOI: 10.1016/j.biopha.2019.109407
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Retraction in
Retraction notice to "Preconditioning with endoplasmic reticulum stress alleviated heart ischemia/reperfusion injury via modulating IRE1/ATF6/RACK1/PERK and PGC-1α in diabetes mellitus" [Biomed. Pharmacother. 118 (2019) 109407].
Yan B, Liu S, Li X, Zhong Y, Tong F, Yang S.Biomed Pharmacother. 2024 Nov 4:117591. doi: 10.1016/j.biopha.2024.117591. Online ahead of print.PMID: 39500697 No abstract available.
Abstract
The purpose of this study was to observe the functions of preconditioning with endoplasmic reticulum stress (ERS) whether alleviated heart ischemia/reperfusion injury (HI/RI) via modulating IRE1/ATF6/RACK1/PERK and PGC-1α expressions in diabetes mellitus (DM) or not. Diabetic rats were pretreated with 0.6 mg/kg tunicamycin (TM, 0.6 mg/kg tunicamycin was administered via intraperitoneal injection 30 minutes prior to the I/R procedures), and then subjected to 45 minutes of ischemia and 3 hours of reperfusion. Blood and myocardial tissues were collected, myocardial pathological injuries were investigated, serum creatine kinase-MB (CK-MB) and cardiac troponin T (cTnT) levels were measured, left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), maximum rate of left ventricular pressure rise (+dp/dtmax) and maximum rate of left ventricular pressure drop (-dp/dtmax) were evaluated, reactive oxygen species (ROS) and caspase-3 levels were observed, ΔΨm level and ROS expression were measured, and activated transcript factor 6 (ATF6), receptor for activated C kinase 1 (RACK1), PRK-like ER kinase (PERK), glucose regulated protein 78 (GRP78) and peroxisome proliferator-activated receptor γ co-activator 1-α (PGC-1α) expressions were assessed. The TM ameliorated the pathological damages, reduced myocardial oxidative stress damages, restrained apoptosis, and upregulated the expressions of ATF6, RACK1, PERK, GRP78 and PGC-1α compared with those of the ischemia/reperfusion (I/R) group in DM. This study suggested the preconditioning with endoplasmic reticulum stress (TM) strategy that could enhance protection against HI/RI in DM in clinical myocardial diseases.
Keywords: DM; HI/RI; IRE1/ATF6/RACK1/PERK; PGC-1α; TM.
参考链接：https://pubpeer.com/publications/E4AE24E575A9AA8226FF820FB81041
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