Angiogenesis in Wound Healing following Pharmacological and Toxicological Exposures

Purpose of Review Toxicological and pharmacological exposures may accelerate or impede wound healing and tissue repair. These exposures impact the wound healing cascade and steps within the process including (1) hemostasis, (2) the inflammatory stage, (3) proliferation, and (4) maturation. Angiogenesis plays a critical role during the wound healing process via clot invasion and organization of vasculature throughout new connective tissue. This review examines how toxicological insults and pharmacotherapeutics impact the tissue healing process. We focus on four primary environmental exposures, namely, radiation, pharmacotherapeutics, metals, and dioxins for the scope of this review. Recent Findings Recent literature suggests that individuals with comorbidities such as autoimmune disorders or cardiometabolic diseases are most susceptible to angiogenic delays and wound healing deficits following toxicological or pharmacological insult. As newer drug-delivery systems and pharmaceutics become available, exposures to these compounds have led to improved wound healing by impacting molecular angiogenic pathways. Environmental and medical exposures from radiological or persistent pollutants may impede wound healing via these angiogenic factors. Summary These data suggest that environmental exposures via metals, dioxins, exogenous radiation, or pharmaceutics will ultimately promote or diminish molecular angiogenic factors, such as vascular endothelial growth factor (VEGF), and impact the wound healing cascade.