Lu Wei,1 Buxin Zhang,2 Yuanhui Tu,2 Aimin Liu1,2 

1The Second Clinical Medical College, Henan University of Chinese Medicine, Zhengzhou, Henan, People’s Republic of China; 2Department of Dermatology, Henan Province Hospital of Traditional Chinese Medicine (the Second Affiliated Hospital of Henan University of Chinese Medicine), Zhengzhou, Henan, People’s Republic of China

Correspondence: Aimin Liu, Department of Dermatology, Henan Province Hospital of Traditional Chinese Medicine, The Second Affiliated Hospital of Henan University of Chinese Medicine, No. 6, Dongfeng Road, Jinshui District, Zhengzhou City, Henan Province, 450053, People’s Republic of China, Tel +86 13592603226, Fax +86-0371-60973329, Email hnzylam@126.com

Abstract: Psoriasis is a chronic inflammatory disease with a complex pathogenesis. Hyperplasia of glycolytic-dependent epidermal keratinocytes (KCs) is a new hallmark of psoriasis pathogenesis. Meanwhile, immune cells undergo metabolic reprogramming similar to KCs. Glycolysis provides energy for the proliferation of KCs, while it also releases lactic acid to facilitate the differentiation of immune cells. In turn, differentiated immune cells further promote KCs glycolysis by releasing inflammatory factors, thus forming an immunometabolism loop. The interaction between immune response and metabolic pathways jointly promotes the sustained proliferation of KCs and the secretion of various inflammatory factors by immune cells. Understanding the role of glycolysis in immunometabolism of psoriasis may provide new ideas for non-immunosuppressive treatment of psoriasis. This article aims to review the role of glycolysis in the pathogenesis of psoriasis and attempts to summarize the key enzymes and regulatory factors involved in psoriasis glycolysis, as well as their interactions. Finally, we discuss the pharmacological modulators of glycolysis in psoriasis.

Keywords: psoriasis, keratinocytes, glycolysis, metabolic reprogramming, immunometabolism