Figure 1.

Schematic depicting the inflammatory cascade seen in rosacea. Increased cathelicidin and KLK5 levels lead to the proinflammatory and pro-angiogenic states seen in rosacea. Over time, vascular proliferation progresses leading to altered cutaneous vasculature characterized by an increase in the number and caliber of superficial cutaneous blood vessels. These vascular changes, which develop over time, appear to account for telangiectasia formation and diffuse persistent facial erythema of rosacea that worsens during a flare and persists between flares of the rosacea.