Gtf2h4, also known as general transcription factor IIH subunit 4, is involved in transcription-dependent DNA repair mechanisms [2]. It may play a role in regulating gene expression, which is crucial for maintaining genomic integrity and normal cellular functions.

In ischemic diseases, Gtf2h4 has been shown to regulate partial endothelial-to-mesenchymal transition (EndMT) via NF-κB activation through NCOA3 phosphorylation. In vivo experiments confirmed that Gtf2h4 significantly promoted partial EndMT and angiogenesis after ischemic injury [1].

In prostate cancer, high expression of Gtf2h4 is associated with a higher biochemical recurrence rate, indicating it may be a risk factor for poor prognosis [4]. Also, a genetic variant in Gtf2h4 has been associated with lung cancer risk, where the variant allele was significantly associated with decreased DNA repair capacity phenotype and decreased mRNA expression levels [3].

In summary, Gtf2h4 is important in DNA repair-related functions and has significant implications in diseases such as ischemic diseases, prostate cancer, and lung cancer. The findings from in vivo studies in ischemic injury models and genetic association studies in cancer patients highlight its role in disease-related biological processes, providing potential therapeutic targets for these diseases.