The Myeloid Mineralocorticoid Receptor Regulates Dermal Angiogenesis and Inflammation in Glucocorticoid-Induced Impaired Wound Healing

The study explored the role of the mineralocorticoid receptor (MR) in glucocorticoid-induced impaired wound healing, particularly its effects on angiogenesis and inflammation. It was found that MR activation in myeloid cells contributed to delayed wound healing by prolonging inflammation and impairing angiogenesis. The use of MR antagonists, such as canrenoate, improved healing by enhancing dermal angiogenesis and promoting a switch in macrophages from a pro-inflammatory to an anti-inflammatory phenotype. The research suggested that targeting MR in myeloid cells could be a therapeutic strategy to improve wound healing in glucocorticoid-treated skin, highlighting the potential of topical MR inhibitors for patients with delayed healing due to glucocorticoid treatments.