This suggests that SS can result from microcirculatory dysfunction [31] due to steatosis, dysfunction of the microvessels, and the effects of vasoactivators (e.g., angiotensin and inducible NO synthase (iNOS)), hormones (e.g., endothelin), and cytokines (e.g., tumor necrosis factor-α) [32–34]. Here, TNF is linked to steatosis.