PTMA, short for prothymosin alpha, is a protein-coding gene with significant biological functions. It is involved in various cellular processes such as cell proliferation, differentiation, and apoptosis. PTMA has been shown to play a role in regulating mitochondrial oxidative phosphorylation through binding to HMGB1, thus affecting the malignant progression of esophageal squamous cell carcinoma (ESCC) [1]. It also appears to be related to fibrosis-related processes, as it is positively correlated with TGFβ1 and SMAD4 in oral submucous fibrosis, and its knockdown or overexpression can reverse or enhance TGFβ1-induced fibrosis in primary human oral submucous fibroblasts respectively [2].

In studies related to diseases, in ESCC, PTMA expression is abnormally elevated, and its inhibition can decrease ESCC cell activity and increase apoptosis, potentially through inhibiting mitochondrial oxidative phosphorylation by binding to HMGB1 [1]. In oral submucous fibrosis, PTMA is a newly identified autoantigen, and targeting it might be a promising treatment strategy [2]. In chronic apical periodontitis, PTMA upregulation moderates the inflammatory response and prevents macrophage osteoclastogenesis, providing a basis for targeted therapeutic strategies [3]. Also, in the context of HIV-1 infection, PTMA has been identified as a host factor that restricts HIV-1 transcription and infectious virus production in vivo [4].

In conclusion, PTMA plays crucial roles in multiple biological processes and disease conditions. Its functions in cancer development, fibrosis, and immune-related diseases have been revealed through various studies. Understanding PTMA provides insights into the mechanisms of these diseases and may offer potential targets for therapeutic interventions.