Page 373 - Read Online

Yang et al. Plast Aesthet Res 2020;7:34 I http://dx.doi.org/10.20517/2347-9264.2020.24 Page 3 of 10

Figure 1. Three possible pathways that may explain how stress hormones (NE, E) could induce abnormal cytokine profiles and
inflammatory responses. TGF: transforming growth factor; TNF: tumor necrosis factor; AR: adrenergic receptors; IL: interleukin; NE:
norepinephrine; E: epinephrine

HYPOTHESIS
The psychological and mental state of keloid patients has been investigated and observed in clinical
practice, but unfortunately, the association between the psychological stress-induced pathological
alterations in keloids has been neglected. Based on the published literature, we propose the hypothesis that
psychological stress can be a risk factor of keloid development as stress hormones (NE, E) might contribute
to keloid pathogenesis [Figure 1]. Therefore, attenuating the AR-receptor function(s) may enhance the
efficacy of traditional keloid treatments and reduce the therapeutic resistance. The following sections
provide a detailed description of the hypothesis with related supporting evidence from the literature.

EVALUATIONS OF THE HYPOTHESIS: THE PROMOTING EFFECT OF PSYCHOLOGICAL
STRESS ON KELOID PATHOGENESIS
Stress hormones could increase IL-6 expression to enhance fibrosis via activating β-ARs
[15]
As a critical mediator of fibrosis [11-14] and inflammation , elevated IL-6 level has been identified in both
keloid tissues and psychologically stressed population. Other studies revealed that the stress hormones