5-Methoxytryptophan attenuates postinfarct cardiac injury by controlling oxidative stress and immune activation

WAN-TSENG HSUTseng, Ya-HsuanYa-HsuanTsengJui, Hsiang-YiangHsiang-YiangJuiKuo, Chen-ChinChen-ChinKuoWu, Kenneth K.Kenneth K.WuCHII-MING LEE2021-07-162021-07-162021222828https://www.scopus.com/inward/record.uri?eid=2-s2.0-85107287456&doi=10.1016%2fj.yjmcc.2021.05.014&partnerID=40&md5=18eb18fdabd8469e48b7d48b1aef4e3chttps://scholars.lib.ntu.edu.tw/handle/123456789/571581Aims: Myocardial infarction (MI) remains a major cause of heart failure. 5-Methoxytryptophan (5-MTP), a 5-methoxyindole metabolite of L-tryptophan, exerts anti-inflammatory and antifibrotic effects, but MI impairs the biosynthesis of cardiac 5-MTP. Therefen5-Methoxytryptophan; Inflammation; Myocardial infarction; NADPH oxidase; Oxidative stress[SDGs]SDG35 methoxytrptophan; caspase 3; CD11b antigen; interleukin 1; interleukin 18; interleukin 6; monocyte chemotactic protein 1; RANTES; reduced nicotinamide adenine dinucleotide phosphate oxidase; tryptophan derivative; unclassified drug; 5-methoxytryptophan;5-Methoxytryptophan attenuates postinfarct cardiac injury by controlling oxidative stress and immune activationjournal article10.1016/j.yjmcc.2021.05.014340871952-s2.0-85107287456