Rosacea is a common, chronic inflammatory disorder of the skin, with central facial erythema and inflammatory papules and pustules as the commonly recognized features. Although the exact pathogenesis of rosacea is unknown, dysregulation of the innate immune system, neurovascular dysregulation and overgrowth of commensal skin organisms are thought to be involved in the pathophysiology of rosacea. Various receptors and mediators, including cathelicidin, endoplasmic reticulum(ER) stress, toll-like receptor(TLR) 2, protease-activated receptor(PAR) 2, transient receptor potential(TRP)s, and mast cells, express important functions in each aspect. They are also intimately connected and form a proinflammatory cascade, which ultimately results in the development of clinical symptoms presented in rosacea. In this review, we briefly summarize key factors and recent studies about the updated pathogenesis of rosacea.