Txn1, encoding thioredoxin-1, is a major cellular antioxidant in mammals. It regulates the dithiol/disulfide balance of interacting proteins, playing a crucial role in the defense against oxidative stress [4,5]. Thioredoxin-1 is involved in a wide range of physiological cellular responses, and its function is closely related to intracellular redox homeostasis [4].

In the context of intracerebral hemorrhage (ICH), Txn1 was identified as a distinctively expressed RNA-binding protein. Overexpression of Txn1 in an ICH rat model reduced secondary injury and improved outcomes, and it binds to inflammation-and apoptosis-related mRNAs, affecting gene expression [1]. In a binary rat model of hypo-and hyperthyroidism, the relative expression of Txn1 increased significantly in both hypothyroid and hyperthyroid groups compared to the control group, and treatment with gallic acid decreased its expression [2]. In a study on liver fibrosis in rats, Txn1 was one of the key proteins in the combination therapy with taurine, epigallocatechin gallate and genistein [3]. In murine hematopoietic stem cells, deletion of Txn1 activated the TP53 signaling pathway and attenuated the cells' capacity to reconstitute hematopoiesis, while recombinant Txn1 promoted their proliferation and expansion [4]. In rats with a Txn1-F54L mutation, bilateral symmetrical vacuolar degeneration was observed in the midbrain, suggesting Txn1's role in reducing oxidative stress in midbrains with high energy metabolism [5].

In summary, Txn1 is essential for maintaining redox balance and is involved in multiple biological processes. Studies using various animal models, especially gene-knockout-related models, have revealed its role in diseases such as ICH, thyroid disorders, liver fibrosis, and hematopoietic stem cell regulation, as well as its importance in protecting the midbrain from oxidative stress-induced degeneration.