Tgfb3, short for transforming growth factor beta 3, is a key member of the transforming growth factor beta superfamily, which is an important mediator of tissue repair [4,5]. It has been implicated in multiple biological processes, such as wound healing, fibrosis, and tissue homeostasis maintenance. Tgfb3 may promote scarless healing in the fetus and reduced scarring in adults, potentially offering a scar-reducing therapy [4]. It also plays a role in fibrosis, with its expression increased in human lung and liver fibrotic tissues compared to healthy control tissues [5].

In a family with mandibular coronoid process hyperplasia (CPH), compound heterozygous mutations in the TGFB3 gene were found, suggesting a possible correlation between TGFB3 gene mutations and CPH [1]. In zebrafish, knockout of homologous tgfb3 resulted in a chordoma-like neoplasm, indicating that down-regulation of Tgfb3 causes chordomagenesis [2]. In zebrafish retina, Tgfb3 inhibits injury-dependent Müller glia (MG) proliferation, and inhibition of related signaling pathways rescues MG proliferation in Tgfb3 overexpressing zebrafish [3]. In liver fibrosis mouse models, Tgfb3 was identified as a key driving factor at the tipping point of significant fibrosis transition, promoting fibrogenic genes and down-regulating Mmp13 [6].

In conclusion, Tgfb3 is crucial in processes like wound healing, fibrosis, and tissue development. Gene knockout and animal models, such as zebrafish and mice, have revealed its role in various disease-related conditions, including CPH, chordoma, retina regeneration, and liver fibrosis. Understanding Tgfb3 can potentially provide new insights into disease mechanisms and therapeutic strategies for these conditions.