Cebpd, also known as CCAAT/enhancer-binding protein delta, is a transcription factor belonging to the CEBP family. It modulates diverse biological processes, and its functions are context-and cell-type-dependent. Cebpd is involved in multiple pathways such as EGFR/PI3K, JAK-STAT, and is associated with various biological activities like cell growth, invasion, immune response, oxidative stress, and inflammation [1,2,3].

In glioblastoma, Cebpd is a master transcriptional factor for hypoxia-regulated proteins. Knockdown of Cebpd in GBM cells impairs their invasion and growth capacity, especially under hypoxic conditions, as it activates the EGFR/PI3K pathway through extracellular matrix-integrin mediated EGFR phosphorylation [1].

In urothelial carcinoma, genomic amplification of Cebpd drives its overexpression, which promotes tumorigenesis through multiple pathways such as stabilizing MYC protein, enhancing glycolysis, and inducing angiogenesis and metastasis [2].

In hypertensive cardiac remodeling, Cebpd is reduced, and its upregulation alleviates oxidative stress and inflammation, improving cardiac function [4].

In ischemic stroke, knockdown of Cebpd in a rat model reduces neurological deficits, infarct size, and oxidative stress, while promoting Nrf2/HO-1 pathway activation [5].

In renal ischemia-reperfusion injury, inactivation of Cebpd in mice represses hypoxia-induced FN-1 expression and reduces macrophage accumulation [6].

In conclusion, Cebpd plays crucial roles in multiple biological processes and diseases. Through gene-knockout or conditional-knockout mouse models and other loss-of-function experiments, its functions in glioblastoma, urothelial carcinoma, hypertensive cardiac remodeling, ischemic stroke, and renal ischemia-reperfusion injury have been revealed. These findings contribute to understanding the disease mechanisms and may provide potential therapeutic targets.