| First Author | Oldknow KJ | Year | 2013 |
| Journal | Endocrinology | Volume | 154 |
| Issue | 3 | Pages | 1310-20 |
| PubMed ID | 23407452 | Mgi Jnum | J:196460 |
| Mgi Id | MGI:5488542 | Doi | 10.1210/en.2012-1886 |
| Citation | Oldknow KJ, et al. (2013) Follistatin-like 3 (FSTL3) mediated silencing of transforming growth factor beta (TGFbeta) signaling is essential for testicular aging and regulating testis size. Endocrinology 154(3):1310-20 |
| abstractText | Follistatin-like 3 (FSTL3) is a glycoprotein that binds and inhibits the action of TGFbeta ligands such as activin. The roles played by FSTL3 and activin signaling in organ development and homeostasis are not fully understood. The authors show mice deficient in FSTL3 develop markedly enlarged testes that are also delayed in their age-related regression. These FSTL3 knockout mice exhibit increased Sertoli cell numbers, allowing for increased spermatogenesis but otherwise showing normal testicular function. The data show that FSTL3 deletion leads to increased AKT signaling and SIRT1 expression in the testis. This demonstrates a cross-talk between TGFbeta ligand and AKT signaling and leads to a potential mechanism for increased cellular survival and antiaging. The findings identify crucial roles for FSTL3 in limiting testis organ size and promoting age-related testicular regression. |
