The role of vasoactive peptides in skin homeostasis—focus on adiponectin and the kallikrein-kinin system

Author:

Souza-Silva Igor M.1ORCID,Steckelings U. Muscha1ORCID,Assersen Kasper Bostlund12ORCID

Affiliation:

1. Department of Cardiovascular & Renal Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark

2. Department of Dermatology, Odense University Hospital, Odense, Denmark

Abstract

Vasoactive peptides often serve a multitude of functions aside from their direct effects on vasodynamics. This article will review the existing literature on two vasoactive peptides and their involvement in skin homeostasis: adiponectin and—as the main representative of the kallikrein-kinin system—bradykinin. Adiponectin is the most abundantly expressed adipokine in the human organism, where it is mainly localized in fat depots including subcutaneous adipose tissue, from where adiponectin can exert paracrine effects. The involvement of adiponectin in skin homeostasis is supported by a number of studies reporting the effects of adiponectin in isolated human keratinocytes, sebocytes, fibroblasts, melanocytes, and immune cells. Regarding skin pathology, the potential involvement of adiponectin in psoriasis, atopic dermatitis, scleroderma, keloid, and melanogenesis is discussed in this article. The kallikrein-kinin system is composed of a variety of enzymes and peptides, most of which have been identified to be expressed in the skin. This also includes the expression of bradykinin receptors on most skin cells. Bradykinin is one of the very few hormones that is targeted by treatment in routine clinical use in dermatology—in this case for the treatment of hereditary angioedema. The potential involvement of bradykinin in wound healing, psoriasis, and melanoma is further discussed in this article. This review concludes with a call for additional preclinical and clinical studies to further explore the therapeutic potential of adiponectin supplementation (for psoriasis, atopic dermatitis, wound healing, scleroderma, and keloid) or pharmacological interference with the kallikrein-kinin system (for wound healing, psoriasis, and melanoma).

Funder

Danmarks Frie Forskningsfond

Novo Nordisk Fonden

Publisher

American Physiological Society

Subject

Cell Biology,Physiology

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