The link between hypertension and pathological scarring: does hypertension cause or promote keloid and hypertrophic scar pathogenesis?

Pathological scars, namely, keloids and hypertrophic scars (HSs), are caused by excessive cutaneous wound healing that is characterized by histological extracellular matrix (ECM) accumulation, clinically relevant irritating symptoms, and frequent recurrence after surgical excision. To date, there are few effective and specific treatments. This partly reflects the poor understanding of the etiology of these scars and the lack of a suitable animal model. Systemic hypertension has been suggested to participate in pathological scarring. The evidence that supports this hypothesis is reviewed here. Thus, hypertension associates with changes that resemble the aberrant cutaneous wound-healing phases that characterize pathological scar development. It also associates with profibrotic functional changes in the cells that constitute keloids and HSs (endothelial cells, pericytes/myofibroblasts, dermal fibroblasts, and mast cells) and profibrotic ECM remodeling. These hypertension-associated changes are mediated to some extent by inflammation, hypoxia, and the angiotensin/renin-angiotensin-aldosterone system. Thus, hypertension may be an aggravating/risk factor for keloids and HSs. This will help to identify patients who are prone to heavy scars after surgery or postsurgical recurrence. Moreover, pharmacological agents for the prophylaxis and treatment of hypertension-induced fibrosis in other organs may also be useful for keloids/HSs.