Angiocrine factors, mediating the endothelial-mural cell interaction in vascular wall construction as well as maintenance, are incompletely characterized. Recently, Prof. Yulong He’s group fromCyrus Tang Hematology Center, used conditional knockout mouse models, showed that loss of endothelial cell–derived FSTL1 (follistatin-like protein 1) in endothelial cells (Fstl1^ECKO) led to an increase of pulmonary vascular resistance, resulting in the heart regurgitation especially with tricuspid valves. Moreover, there was excessive αSMA (α-smooth muscle actin) associated with atrial endocardia, heart valves, veins, and microvessels after the endothelial FSTL1 deletion. There was also an increase in collagen deposition in livers of Fstl1^ECKO mutants. The SMAD3 (mothers against decapentaplegic homolog 3) phosphorylation (pSMAD3) was significantly enhanced, and pSMAD3 staining was colocalized with αSMA in vein walls, suggesting the activation of TGFβ (transforming growth factor β) signaling in vascular mural cells of Fstl1^ECKO mice. Consistently, treatment with a TGFβ pathway inhibitor reduced the abnormal association of αSMA with the atria and blood vessels in Fstl1^ECKO mutant mice. These findings imply that endothelial FSTL1 is critical for the homeostasis of vascular walls, and its insufficiency may favor cardiovascular fibrosis leading to heart failure. Their work has been published inArteriosclerosis, Thrombosis, and Vascular Biology (Arterioscler Thromb Vasc Biol,2020, 40:958–972)., titled as “Angiocrine FSTL1 (Follistatin-Like Protein 1) Insufficiency Leads to Atrial and Venous Wall Fibrosis via SMAD3 Activation”.

Link to Paper：https://www.ahajournals.org/doi/full/10.1161/ATVBAHA.119.313901?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed&

Link to Prof. He’ group：http://tangcenter.suda.edu.cn/cn/ShowSingleFaculty.aspx?id=26