LNK/SH2B3 loss of function increases susceptibility to murine and human atrial fibrillation.
Matthew B MurphyZhenjiang YangTuerdi SubatiEric Farber-EgerKyungsoo KimDaniel J BlackwellMatthew R FlemingJoshua M StarkJoseph C Van AmburgKaylen K WoodallJustin P Van BeusecumVineet AgrawalCharles D SmartAshley PitzerJames B AtkinsonAgnes B FogoJulie A BastaracheAnnet KiraboQuinn S WellsMeena S MadhurJoey V BarnettKatherine T MurrayPublished in: Cardiovascular research (2024)
These findings identify a novel role for LNK in the pathophysiology of AF in both experimental mice and humans. Moreover, reactive lipid dicarbonyls are critical to the inflammatory AF substrate in Lnk-/- mice and mediate the pro-arrhythmic effects of pro-inflammatory cytokines, primarily through electrical remodelling.
Keyphrases
- atrial fibrillation
- high fat diet induced
- endothelial cells
- catheter ablation
- left atrial
- oral anticoagulants
- left atrial appendage
- anti inflammatory
- direct oral anticoagulants
- heart failure
- oxidative stress
- induced pluripotent stem cells
- fatty acid
- insulin resistance
- metabolic syndrome
- pluripotent stem cells
- wild type
- acute coronary syndrome
- mitral valve
- skeletal muscle
- amino acid