Arrhythmias & electrophysiology

Spexin Diminishes Atrial Fibrillation Vulnerability by Acting on Galanin Receptor 2

CirculationPublished Mechanistic study

Authors' conclusion

Spexin reduces atrial fibrillation susceptibility by inhibiting CREB phosphorylation and thus downregulating KCNJ2 and SLN transcription by GALR2 receptor.

Study context

Population
Patients with and without atrial fibrillation (AF); Spexin knockout (SPX-KO), GALR-cKO and Ang-II-infused mice

Main finding

As reported in the abstract

  • Lower plasma spexin in patients with AF than in subjects without AF
  • Spexin knockout increased AF susceptibility in mice
  • SPX-KO atrium: KCNJ2 and sarcolipin (SLN) upregulated; IK1 current increased and Ca2+ handling impaired in atrial myocytes
  • GALR2-cKO, but not GALR1-cKO or GALR3-cKO, mice had higher AF incidence, with higher IK1 current and intracellular Ca2+ overload
  • CREB phosphorylation upregulated in atria of SPX-KO and GALR2-cKO mice; p-CREB recruited to KCNJ2 and SLN proximal promoters
  • Spexin treatment suppressed CREB signalling, decreased IK1 and intracellular Ca2+ overload, and reduced AF inducibility in Ang-II-infused mice

Original publication

Spexin Diminishes Atrial Fibrillation Vulnerability by Acting on Galanin Receptor 2. Circulation. Published 10 May 2024. doi:10.1161/circulationaha.123.067517

Composed by AI from the published abstract and checked against it. How Briefs are made →

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