Melasma is a common refractory acquired pigmentary skin disease that mainly affects middle-aged women. The pathogenesis of melasma is still uncertain, while abnormal vascular endothelial cells may play a role. We previously demonstrated the yellow light of light-emitting diodes (LED) could inhibit melanogenesis through the photobiomodulation (PBM) of melanocytes and keratinocytes. In the current study, we investigated the effect of 590 nm LED on the function of human microvascular endothelial cells (HMEC-1). We revealed 0–40 J/cm2 590 nm LED had no toxic effect on HMEC-1 in vitro. 590 nm LED irradiation significantly reduced cell migration, tube formation, as well as the expression of vascular endothelial growth factor (VEGF) and stem cell factor (SCF), a pro-melanogenic factor. Moreover, we illustrated that 590 nm LED inhibited the phosphorylation of the AKT/PI3K/mTOR signaling pathway, and the inhibitory effect on HMEC-1 could be partially reversed by insulin-like growth factor 1 (IGF-1), an AKT/PI3K/mTOR pathway agonist. Besides, we conducted a pilot clinical study and observed a marked improvement on facial erythema and pigmentation in melasma patients after amber LED phototherapy. Taken together, 590 nm LED inhibited HMEC-1 migration, tube formation and the secretion of VEGF and SCF, predominantly through the inhibition of the AKT/PI3K/mTOR pathway, which may serve as a novel therapeutic option for melasma.

Vitiligo is an acquired disfiguring disorder caused by melanocyte (MC) destruction, clinically featured by depigmented maculae and/ or patches on skin. The incidence of vitiligo is 0.5%-2.0% worldwide (Krüger & Schallreuter, 2012). Although vitiligo does not affect the survival of patients, it can bring social pressure (Salman et al., 2016) and cause mental diseases (Osinubi et al., 2017), which greatly impairs general health and social lives of patients. Thus, it is of great significance to carry out in-depth studies on the pathogenesis of vitiligo and explore new molecular markers and more effective therapeutic targets. Over the past decades, various pathogenesis hypotheses of vitiligo have been proposed including neural theory, oxidative stress theory, autoimmune hypothesis, intrinsic theory, melanocytorrhagy hypothesis (Gauthier et al., 2003), and integrated theory, all of which acknowledged the damage of MCs as

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