Aldoa, also known as aldolase A, is a crucial glycolytic enzyme. It catalyzes the breakdown of fructose-1,6-bisphosphate to glyceraldehyde 3-phosphate and dihydroxyacetone phosphate in the glycolytic pathway. Glycolysis is fundamental for energy production in cells, and Aldoa's role in this pathway is vital for maintaining normal cellular metabolism. Dysregulation of Aldoa has implications for various biological processes and disease conditions [1-10].

In cancer, Aldoa has been shown to play significant roles. In colon cancer, the POU2F1-ALDOA axis promotes cell proliferation and chemoresistance by enhancing glycolysis and the pentose phosphate pathway activity [1]. In retinoblastoma, Aldoa is overexpressed across diverse cell types. Its knockdown diminishes cell viability, impedes colony formation, and induces metabolic alterations [2]. In breast cancer, an alternative splicing event in Aldoa confers tamoxifen resistance [3]. In prostate cancer, higher Aldoa expression is associated with postoperative metastasis and biochemical recurrence, and its inhibition can suppress cell proliferation [6]. In pancreatic cancer, Aldoa inhibits cell cycle arrest induced by DNA damage via the ATM-PLK1 pathway, promoting cancer development [7]. In addition, in vascular calcification, the orphan nuclear receptor NR4A3 enhances glycolysis activity by directly binding to the promoter regions of Aldoa, promoting medial calcification [4]. In cardiomyocytes, Aldoa protects against hypoxia/reperfusion-induced apoptosis and oxidative stress by regulating the VEGF/Notch 1/Jagged 1 pathway [5].

In conclusion, Aldoa is a key enzyme in the glycolytic pathway, and its dysregulation is associated with multiple diseases, especially various cancers. Studies using different models, including cell-based and in vivo models, have revealed its diverse roles in disease-related biological processes such as cell proliferation, drug resistance, and metabolic reprogramming. Understanding Aldoa's functions provides potential therapeutic targets for treating these diseases.