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the local hypoxia conditions; and (4) dysregulating immune systems to provide an inflammatory
microenvironment that is in favor of keloid formation, thus promoting keloid pathogenesis.

Although the impact of psychological stress on the pathogenesis of diseases, such as cancers, has been
known for decades, its relevance and impact concerning keloid pathogenesis and therapy have barely been
studied. Although the stressed state in keloid patients has been well-observed during clinical practice
and demonstrated by investigations in an African population, more direct evidence are required in the
future. For example, current studies have detected elevated adrenergic receptors, but the concentration
and distribution of catecholamines in keloid tissues remain uninvestigated, so are specific cytokines and
immune cells in the targeted population. Clinically, large-scale evaluations of psychological stress among
keloid patients should also be undertaken as a follow up to “as a proof of principle” pilot studies. Moreover,
studies combing α, β-receptor antagonists and anti-depressant medicines with conventional keloid
therapies could be explored in future clinical trials to realize better treatment outcomes.

DECLARATIONS
Author’s contributions
Made substantial contributions to the conception of the hypothesis: Yang YT, Wu XL, Liu W

Availability of data and materials
Not applicable.

Financial support and sponsorship
This work is financially supported by the National Natural Science Foundation (81671921).

Conflict of interest
All authors declared that there are no conflicts of interest.

Ethical approval and consent to participate
Not applicable.

Consent for publication
Not applicable.

Copyright
© The Author(s) 2020.

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