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  • Title: Highly Reactive Isolevuglandins Promote Atrial Fibrillation Caused by Hypertension.
    Author: 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.
    Journal: JACC Basic Transl Sci; 2020 Jun; 5(6):602-615. PubMed ID: 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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