Mineralocorticoid Receptor Antagonists-A New Sprinkle of Salt and Youth.
Skin atrophy and impaired cutaneous wound healing are the recognized side effects of topical glucocorticoid (GC) therapy. Although GCs have high affinity for the glucocorticoid receptor, they also bind and activate the mineralocorticoid receptor. In light of this, one can speculate that some of the GC-mediated side effects can be remedied by blocking activation of the mineralocorticoid receptor. Indeed, according to Nguyen et al., local inhibition of the mineralocorticoid receptor via antagonists (spironolactone, canrenoate, and eplerenone) rescues GC-induced delayed epithelialization and accelerates wound closure in diabetic animals by targeting epithelial sodium channels and stimulating keratinocyte proliferation. These findings suggest that the use of mineralocorticoid receptor antagonists coupled with GC therapy may be beneficial in overcoming at least some of the GC-mediated side effects.
Wound Healing and Regenerative Medicine Research Program, Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA; Graduate Program in Biomedical Sciences, Faculty of Medical Sciences, University of Kragujevac, Kragujevac, Serbia.
Olivera
O
Stojadinovic
Wound Healing and Regenerative Medicine Research Program, Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA.
Linsey E
LE
Lindley
Wound Healing and Regenerative Medicine Research Program, Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA.
Ivan
I
Jozic
Wound Healing and Regenerative Medicine Research Program, Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, Florida, USA; John P. Hussman Institute for Human Genomics, University of Miami Miller School of Medicine, Miami, Florida, USA. Electronic address: mtcanic@med.miami.edu.
Marjana
M
Tomic-Canic
D000279:Administration, Cutaneous; D000818:Animals; D053503:Epithelial Sodium Channels; D005938:Glucocorticoids; D000451:Mineralocorticoid Receptor Antagonists; D011965:Receptors, Glucocorticoid; D018161:Receptors, Mineralocorticoid / Q000187:drug effects; D013148:Spironolactone
D053503:Epithelial Sodium Channels; D005938:Glucocorticoids; D000451:Mineralocorticoid Receptor Antagonists; D011965:Receptors, Glucocorticoid; D018161:Receptors, Mineralocorticoid; D013148:Spironolactone