Linking atrial fibrillation with non-alcoholic fatty liver disease: potential common therapeutic targets

Abstract

Non-alcoholic fatty liver disease (NAFLD) and atrial fibrillation (AF) are common chronic non-infectious diseases with rising incidences. NAFLD is an independent risk factor for the onset of AF, after adjusting potentially related factors. The pathogenesis of these diseases share several mechanisms including reduced adiponectin level, insulin resistance, and renin angiotensin aldosterone system (RAAS) activation, in addition to activation of common disease pathways that promote inflammation, oxidative stress, and fibrosis. Furthermore, statins and RAAS blockers exert therapeutic effects concurrently on NAFLD and AF. The common pathogenesis of NAFLD and AF may serve as a potential therapeutic target in the future.

Keywords: adiponectin; atrial fibrillation; insulin resistance; non-alcoholic fatty liver disease; renin angiotensin aldosterone system.

Figure 1. The roles of adiponectin, inflammatory cytokines, AngII and insulin resistance in the pathogenesis of NAFLD and AF

NAFLD: non-alcoholic fatty liver disease; AngII: angiotensin II; AT1: angiotensin II type 1; TNF-α: tumor necrosis factor-α; IL: interleukin; IFN-γ: interferon-γ; FFA: free fat acid; AMPK: adenosine monophosphate-activated protein kinase; ACC: acetyl-CoA carboxylase; IKK: inhibitor of nuclear factor kappa-B kinase; JNK: c-Jun N-terminal kinase; AP-1: Activator Protein-1; PPAR: peroxisome proliferator-activated receptor; PGC-1: PPAR γ coactivator-1; NF-κB: nuclear factor κ-light-chain-enhancer of activated B cells.