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 in humans. Moreover, reactive lipid dicarbonyls are critical to the inflammatory AF substrate in Lnk-/- mice and mediate the proarrhythmic effects of pro-inflammatory cytokines, primarily through electrical remodeling.