FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3088589624> ?p ?o ?g. }

• W3088589624 endingPage "165980" @default.
• W3088589624 startingPage "165980" @default.
• W3088589624 abstract "Leucine, isoleucine, and valine are diet derived and essential amino acids that are termed branched-chain amino acids (BCAA). BCAA are widely used as dietary supplements to boost muscle growth and enhance exercise performance. However, the effects of BCAA on myocardial function are largely unknown. This study was designed to investigate whether BCAA affect heart function and, if so, to further explore the underlying molecular basis for the observed effects. C57BL/6J mice were randomly divided into two groups, the control group received solvent (water) and the BCAA group received 2% BCAA dissolved in water, for a successive period of 12 weeks. Compared with control, BCAA treatment significantly increased water consumption without changing body weight or diet consumption; heart tissue BCAA levels were increased, markers representative of myocardial injury in heart tissue including c-reactive protein and cardiac muscle troponin were increased ; and creatine kinase, creatine kinase-MB, and lactate dehydrogenase were increased in serum; severe myocardial fibrosis was observed by Masson staining, which was accompanied by increased reactive oxygen species (ROS) production and decreased superoxide dismutase activity in heart tissue; both p-AMPK and p-ULK1 were significantly increased as was autophagy, judged by the presence of LC3 by western blotting and immunofluorescence, increased numbers of autophagosomes were found by transmission electron microscopy in the BCAA group. In vitro, 20 mmol/L BCAA significantly decreased cell viability and increased the production of ROS, as well as the expression of p-AMPK/AMPK and p-ULK1/ULK1 in cultured H9C2 cells. Treatment with the ROS scavenger N-acetyl-L-cysteine (NAC) improved cell viability and reversed ROS changes. Decreased H9C2 cell viability induced with 20 mmol/L BCAA was reversed by either blocking AMPK or inhibition of ULK1. Furthermore, blocking AMPK significantly decreased p-ULK1/ULK1, while inhibition of ULK1 reversed the enhanced expression of LC3-II/LC3-I induced by BCAA. Excessive ROS production and decreased cell viability induced by BCAA were further confirmed in primary cultured murine cardiomyocytes. Pharmacological activation of α7nAChR with PNU-282987 attenuated BCAA-induced injury in primary murine cardiomyocytes. However, this compound failed to suppress BCAA activation of AMPK and autophagy (LC3-II/I ratio). These results provide the first evidence that treatment of mice with BCAA induced myocardial injury by triggering excessive ROS production and by enhancing AMPK-ULK1 pathway-dependent autophagy. These findings suggested that inhibition of either ROS production or autophagy may alleviate myocardial injury induced by BCAA." @default.
• W3088589624 created "2020-10-01" @default.
• W3088589624 creator A5040149743 @default.
• W3088589624 creator A5049152441 @default.
• W3088589624 creator A5051368106 @default.
• W3088589624 creator A5063967701 @default.
• W3088589624 creator A5065502701 @default.
• W3088589624 creator A5067383399 @default.
• W3088589624 creator A5077388601 @default.
• W3088589624 creator A5081919984 @default.
• W3088589624 creator A5082875974 @default.
• W3088589624 date "2021-01-01" @default.
• W3088589624 modified "2023-10-17" @default.
• W3088589624 title "Excessive ROS production and enhanced autophagy contribute to myocardial injury induced by branched-chain amino acids: Roles for the AMPK-ULK1 signaling pathway and α7nAChR" @default.
• W3088589624 cites W1544109218 @default.
• W3088589624 cites W1864635191 @default.
• W3088589624 cites W1970637701 @default.
• W3088589624 cites W1973472942 @default.
• W3088589624 cites W1994343244 @default.
• W3088589624 cites W2014943313 @default.
• W3088589624 cites W2024006151 @default.
• W3088589624 cites W2025665129 @default.
• W3088589624 cites W2036903182 @default.
• W3088589624 cites W2065396708 @default.
• W3088589624 cites W2067600563 @default.
• W3088589624 cites W2081706292 @default.
• W3088589624 cites W2088857580 @default.
• W3088589624 cites W2091210052 @default.
• W3088589624 cites W2143765047 @default.
• W3088589624 cites W2145206598 @default.
• W3088589624 cites W2202487473 @default.
• W3088589624 cites W2282883825 @default.
• W3088589624 cites W2317552858 @default.
• W3088589624 cites W2319656552 @default.
• W3088589624 cites W2340330396 @default.
• W3088589624 cites W2470621842 @default.
• W3088589624 cites W2520673124 @default.
• W3088589624 cites W2530466621 @default.
• W3088589624 cites W2550846703 @default.
• W3088589624 cites W2576580888 @default.
• W3088589624 cites W2617115371 @default.
• W3088589624 cites W2754409876 @default.
• W3088589624 cites W2755578884 @default.
• W3088589624 cites W2761245997 @default.
• W3088589624 cites W2768018305 @default.
• W3088589624 cites W2770335123 @default.
• W3088589624 cites W2794323786 @default.
• W3088589624 cites W2800923282 @default.
• W3088589624 cites W2802787573 @default.
• W3088589624 cites W2883096655 @default.
• W3088589624 cites W2885048546 @default.
• W3088589624 cites W2885179151 @default.
• W3088589624 cites W2885511418 @default.
• W3088589624 cites W2885628701 @default.
• W3088589624 cites W2888165325 @default.
• W3088589624 cites W2888527186 @default.
• W3088589624 cites W2888893480 @default.
• W3088589624 cites W2890125383 @default.
• W3088589624 cites W2892317065 @default.
• W3088589624 cites W2897304981 @default.
• W3088589624 cites W2897452799 @default.
• W3088589624 cites W2898520486 @default.
• W3088589624 cites W2899999651 @default.
• W3088589624 cites W2902139199 @default.
• W3088589624 cites W2902246840 @default.
• W3088589624 cites W2908838876 @default.
• W3088589624 cites W2911945551 @default.
• W3088589624 cites W2915168964 @default.
• W3088589624 cites W2936142442 @default.
• W3088589624 cites W2946442337 @default.
• W3088589624 cites W2947766501 @default.
• W3088589624 cites W2948500091 @default.
• W3088589624 cites W2948863714 @default.
• W3088589624 cites W2955235606 @default.
• W3088589624 cites W2963792141 @default.
• W3088589624 cites W2970028801 @default.
• W3088589624 cites W2973564248 @default.
• W3088589624 cites W2987447558 @default.
• W3088589624 cites W2992015556 @default.
• W3088589624 cites W3002534731 @default.
• W3088589624 cites W3043506937 @default.
• W3088589624 doi "https://doi.org/10.1016/j.bbadis.2020.165980" @default.
• W3088589624 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32980459" @default.
• W3088589624 hasPublicationYear "2021" @default.
• W3088589624 type Work @default.
• W3088589624 sameAs 3088589624 @default.
• W3088589624 citedByCount "34" @default.
• W3088589624 countsByYear W30885896242021 @default.
• W3088589624 countsByYear W30885896242022 @default.
• W3088589624 countsByYear W30885896242023 @default.
• W3088589624 crossrefType "journal-article" @default.
• W3088589624 hasAuthorship W3088589624A5040149743 @default.
• W3088589624 hasAuthorship W3088589624A5049152441 @default.
• W3088589624 hasAuthorship W3088589624A5051368106 @default.
• W3088589624 hasAuthorship W3088589624A5063967701 @default.
• W3088589624 hasAuthorship W3088589624A5065502701 @default.
• W3088589624 hasAuthorship W3088589624A5067383399 @default.
• W3088589624 hasAuthorship W3088589624A5077388601 @default.

• next