Literature DB >> 32001270

Branched-chain amino acids-induced cardiac protection against ischemia/reperfusion injury.

Shiho Satomi1, Atsushi Morio2, Hirotsugu Miyoshi2, Ryuji Nakamura2, Rie Tsutsumi3, Hiroshi Sakaue3, Toshimichi Yasuda2, Noboru Saeki2, Yasuo M Tsutsumi4.   

Abstract

AIMS: Amino acids, especially branched chain amino acids (BCAAs), have important regulatory roles in protein synthesis. Recently studies revealed that BCAAs protect against ischemia/reperfusion (I/R) injury. We studied the signaling pathway and mitochondrial function affecting a cardiac preconditioning of BCAAs. MAIN
METHODS: An in vivo model of I/R injury was tested in control, mTOR+/+, and mTOR+/-. Mice were randomly assigned to receive BCAAs, rapamycin, or BCAAs + rapamycin. Furthermore, isolated cardiomyocytes were subjected to simulated ischemia and cell death was quantified. Biochemical and mitochondrial swelling assays were also performed. KEY
FINDINGS: Mice treated with BCAAs had a significant reduction in infarct size as a percentage of the area at risk compared to controls (34.1 ± 3.9% vs. 44.7 ± 2.6%, P = 0.001), whereas mice treated with the mTOR inhibitor rapamycin were not protected by BCAA administration (42.2 ± 6.5%, vs. control, P = 0.015). This protection was not detected in our hetero knockout mice of mTOR. Western blot analysis revealed no change in AKT signaling whereas activation of mTOR was identified. Furthermore, BCAAs prevented swelling which was reversed by the addition of rapamycin. In myocytes undergoing simulated I/R, BCAA treatment significantly preserved cell viability (71.7 ± 2.7% vs. 34.5 ± 1.6%, respectively, p < 0.0001), whereas rapamycin prevented this BCAA-induced cardioprotective effect (43.5 ± 3.4% vs. BCAA, p < 0.0001). SIGNIFICANCE: BCAA treatment exhibits a protective effect in myocardial I/R injury and that mTOR plays an important role in this preconditioning effect.
Copyright © 2020 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Amino acid; Ischemia; Mitochondria; Reperfusion; mTOR

Year:  2020        PMID: 32001270     DOI: 10.1016/j.lfs.2020.117368

Source DB:  PubMed          Journal:  Life Sci        ISSN: 0024-3205            Impact factor:   5.037


  6 in total

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Journal:  Cells       Date:  2022-05-20       Impact factor: 7.666

Review 2.  The complex network of mTOR signalling in the heart.

Authors:  Sebastiano Sciarretta; Maurizio Forte; Giacomo Frati; Junichi Sadoshima
Journal:  Cardiovasc Res       Date:  2022-01-29       Impact factor: 10.787

3.  Effects of Remimazolam and Propofol on Ca2+ Regulation by Ryanodine Receptor 1 with Malignant Hyperthermia Mutation.

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Journal:  Biomed Res Int       Date:  2021-01-04       Impact factor: 3.411

4.  The Effect of miR-505-5p on Inhibition of Serum Uromodulin Ameliorates Myocardial Inflammation and Apoptosis Induced by Ischemia-Reperfusion.

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Journal:  Oxid Med Cell Longev       Date:  2022-10-03       Impact factor: 7.310

5.  Chronically elevated branched chain amino acid levels are pro-arrhythmic.

Authors:  Vincent Portero; Thomas Nicol; Svitlana Podliesna; Gerard A Marchal; Antonius Baartscheer; Simona Casini; Rafik Tadros; Jorien L Treur; Michael W T Tanck; I Jane Cox; Fay Probert; Tertius A Hough; Sara Falcone; Leander Beekman; Martina Müller-Nurasyid; Gabi Kastenmüller; Christian Gieger; Annette Peters; Stefan Kääb; Moritz F Sinner; Andrew Blease; Arie O Verkerk; Connie R Bezzina; Paul K Potter; Carol Ann Remme
Journal:  Cardiovasc Res       Date:  2022-06-22       Impact factor: 13.081

6.  PHLDA3 inhibition attenuates endoplasmic reticulum stress-induced apoptosis in myocardial hypoxia/reoxygenation injury by activating the PI3K/AKT signaling pathway.

Authors:  Kai Liu; Ying Chen; Fen Ai; Yun-Qian Li; Kun Zhang; Wei-Tong Zhang
Journal:  Exp Ther Med       Date:  2021-04-14       Impact factor: 2.447

  6 in total

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