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Editorial
. 2024 Jul 2;120(8):814-816.
doi: 10.1093/cvr/cvae083.

A mechanistic LNK between inflammation and atrial fibrillation?

Affiliations
Editorial

A mechanistic LNK between inflammation and atrial fibrillation?

Joshua A Keefe et al. Cardiovasc Res. .
No abstract available

PubMed Disclaimer

Conflict of interest statement

Conflict of interest: none declared.

Figures

Figure 1
Figure 1
Lnk deficiency in mice leads to enhanced haematopoiesis, leading to systemic inflammation mediated by TNF-α and IL-1β and subsequent deposition of IsoLG adducts in the atria. IsoLG deposition impairs peak sodium (INa) and transient outward (Ito) potassium currents, leading to APD prolongation and AF. Three-month treatment of mice with dicarbonyl scavenger 2-HOBA rescued AF, and TNF-α and IL-1β inhibition protected against arrhythmogenic electrical remodelling and mitochondrial dysfunction, respectively. This image was created with BioRender.com. 2-HOBA, 2-hydroxybenzylamine; AF, atrial fibrillation; IL-1β, interleukin-1 beta; IsoLG, isolevuglandin; Lnk, lymphocyte adaptor protein; TNF-α, tumour necrosis factor alpha.

Comment on

  • LNK/SH2B3 loss of function increases susceptibility to murine and human atrial fibrillation.
    Murphy MB, Yang Z, Subati T, Farber-Eger E, Kim K, Blackwell DJ, Fleming MR, Stark JM, Van Amburg JC, Woodall KK, Van Beusecum JP, Agrawal V, Smart CD, Pitzer A, Atkinson JB, Fogo AB, Bastarache JA, Kirabo A, Wells QS, Madhur MS, Barnett JV, Murray KT. Murphy MB, et al. Cardiovasc Res. 2024 Jul 2;120(8):899-913. doi: 10.1093/cvr/cvae036. Cardiovasc Res. 2024. PMID: 38377486 Free PMC article.

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