Nonalcoholic fatty liver disease (NAFLD) is now considered the most prevalent chronic liver disease, affecting over 30% of the US adult population. NAFLD is strongly linked to insulin resistance and is considered the hepatic manifestation of the metabolic syndrome. Activation of the renin-angiotensin-aldosterone system (RAAS) is known to play a role in the hypertension observed in the metabolic syndrome and also is thought to play a central role in insulin resistance and NAFLD. Angiotensin II (AngII) is considered the primary effector of the physiological outcomes of RAAS signaling, both at the systemic and local tissue level. Herein, we review data describing the potential involvement of AngII-mediated signaling at multiple levels in the development and progression of NAFLD, including increased steatosis, inflammation, insulin resistance, and fibrosis. Additionally, we present recent work on the potential therapeutic benefits of RAAS and angiotensin II signaling inhibition in rodent models and patients with NAFLD.
Keywords: Angiotensin II; Fibrosis; Mitochondria; NAFLD; Steatosis.
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