Role of Oxidative Stress in Hepatic and Extrahepatic Dysfunctions during Nonalcoholic Fatty Liver Disease (NAFLD)

Figure 3

Extrahepatic tissue complications by nonalcoholic fatty liver disease (NAFLD). In skeletal muscle, sarcopenia is induced by NAFLD. The development of sarcopenia is characterized by muscle weakness and fibrosis. Among the factors that contribute to sarcopenia in NAFLD are the increase of proinflammatory cytokines (tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6)), classical renin-angiotensin system (RAS), myostatin, and ammonium. In cardiac tissue, the main complication induced by NAFLD is cirrhotic cardiomyopathy (CCM). CCM is characterized by systolic and diastolic dysfunction in the ventricle and altered electromechanical patterns. Besides, NAFLD also induces impairment in vascular endothelium, characterized by hemodynamic changes, mainly caused by the increase of classical RAS and represented by the rise in volemia and portal hypertension. NAFLD can induce acute renal failure (ARF) and chronic kidney diseases (CKD) in the renal system. ARF is developed in NAFLD patients with hypovolemia caused by a vasoconstriction response, classical RAS activation, and also activation of the sympathetic nervous system (SNS). CKD is characterized by impaired filtration. This impairment increases creatinine serum levels and induces proteinuria. NAFLD is related to peripheral neuropathy (PN) and hepatic encephalopathy (HE) in the nervous system. PN related to NAFLD is a pathology characterized by altered myelin sheath in peripheral nerves with neuronal loss. The HE causes brain edema and atrophy and is favored by hyperammonemia (HA) in NAFLD. Created with http://BioRender.com