Hpgds, short for hematopoietic prostaglandin D synthase, is responsible for the production of prostaglandin D2 (PGD2), an inflammatory mediator. It is involved in the arachidonic acid metabolism pathway, which is of great biological importance as lipid metabolism is crucial for various physiological processes [1,2,3,4]. Genetic models, such as gene knockout (KO) mouse models, can be valuable for studying Hpgds functions.

Hpgds deficiency in type 2 diabetic mice delays normal wound healing, while overexpressing Hpgds in adipose-derived mesenchymal stem cells accelerates diabetic wound healing by reducing neutrophil and CD8T cell recruitment, promoting M2 macrophage polarization and increasing growth factor production [1]. In A549 cell lines, knockdown of Hpgds promotes lipid synthesis and cell migration, and the knockdown promotes migration response by upregulating the expression of lipid metabolism key enzymes ACSL1 and ACC [2].

In conclusion, Hpgds plays a significant role in wound healing and lipid metabolism-related processes. The findings from KO-like models, such as in diabetic mice and cell lines, contribute to understanding its functions in diabetes-related wound healing and lung adenocarcinoma development, providing potential therapeutic targets for these disease areas.