Dusp26, also known as neuroendocrine-associated phosphatase (NEAP), is an atypical dual-specificity phosphatase. It plays a role in regulating intracellular signaling pathways, especially those related to MAP kinases. It has been implicated in a wide range of physiological processes, including cell growth, differentiation, and neuronal development [2,6].

In disease-related research, gene knockout models have provided insights. In ApoE-/-mice fed a high-cholesterol diet, Dusp26 silencing ameliorated aortic valve calcification, reducing valve thickness, calcium deposition, and osteogenic marker levels [1]. In diabetic cardiomyopathy, Dusp26 expression was downregulated in diabetic db/db mice. Overexpression in these mice improved cardiac function, mitochondrial function, and reduced fibrosis and hypertrophy [3]. In diabetic nephropathy, Dusp26 deficiency in mice accelerated renal injury, fibrosis, and oxidative stress [5]. In glioblastoma cells, decreased Dusp26 expression promoted malignant behavior [4]. In prostate cancer cells, overexpression of Dusp26 inhibited cell proliferation, migration, and invasion [7].

In conclusion, Dusp26 is crucial in multiple biological processes and disease conditions. Gene knockout and overexpression models in mice have revealed its role in aortic valve calcification, diabetic cardiomyopathy, diabetic nephropathy, glioblastoma, and prostate cancer. Understanding Dusp26's functions can potentially lead to new therapeutic strategies for these diseases.