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Highly Reactive Isolevuglandins Promote Atrial Fibrillation Caused by
Authors Prinsen JK, Kannankeril PJ, Sidorova TN, Yermalitskaya LV, Boutaud O,
Zagol-Ikapitte I, Barnett JV, Murphy MB, Subati T, Stark JM, Christopher IL,
Jafarian-Kerman SR, Saleh MA, Norlander AE, Loperena R, Atkinson JB, Fogo AB,
Luther JM, Amarnath V, Davies SS, Kirabo A, Madhur MS, Harrison DG, Murray KT
Submitted By Submitted Externally on 9/28/2020
Status Published
Journal JACC. Basic to translational science
Year 2020
Date Published 6/1/2020
Volume : Pages 5 : 602 - 615
PubMed Reference 32613146
Abstract Oxidative damage is implicated in atrial fibrillation (AF), but antioxidants are
ineffective therapeutically. The authors tested the hypothesis that highly
reactive lipid dicarbonyl metabolites, or isolevuglandins (IsoLGs), are
principal drivers of AF during hypertension. In a hypertensive murine model and
stretched atriomyocytes, the dicarbonyl scavenger 2-hydroxybenzylamine (2-HOBA)
prevented IsoLG adducts and preamyloid oligomers (PAOs), and AF susceptibility,
whereas the ineffective analog 4-hydroxybenzylamine (4-HOBA) had minimal effect.
Natriuretic peptides generated cytotoxic oligomers, a process accelerated by
IsoLGs, contributing to atrial PAO formation. These findings support the concept
of pre-emptively scavenging reactive downstream oxidative stress mediators as a
potential therapeutic approach to prevent AF.


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