The observed reversal of functional capillary density in the hepatic microcirculation by SV may be a consequence of the decrease in (i) steatosis, (ii) fibrosis, (iii) HSC activation and COL1A1 expression and (iv) leukocyte recruitment, which in turn reversed tissue hypoxia and recovered microvascular blood flow. This evidence concerns the gene COL1A1 and steatosis.