国产成人嫩模一区二区|超级黄色网页|兔子先生tz|麻豆文化传媒网站官网污|在线播放欧美日韩精品|爱豆影视传媒免费下载|蜜桃影像传媒av剧情|麻豆文化传媒APP最新iOS|陈可心倩女幽魂爱豆传媒|91国视频产,国产传媒播放,想看三级片,网红吃瓜黑料爆料网反差

Research Interests

• The mechanism of FSTL3 induced calcification of aortic valve interstitial cells in calcific aortic valve disease

• Calcific aortic valve is one of a variety of risk factors for heart diseases, but the pathogenesis is not clear. Now we found that: the expression of FSTL3 is increased in serum and valve interstitial cells of valve tissues of aortic valve calcification, and positive related with age. Sirt1 regulated the expression of FSTL3 in valve interstitial cells. Moreover, FSTL3 promoted the calcification of valve interstitial cells and bind with Activin A and MSTN. The RNA-sequencing assay showed that FSTL3 regulated some genes (such as SOX9) expression and HIF-1α activation. These results hint that FSTL3 regulated valvular interstitial cells calcification process via multiple signaling pathways, which is an important mechanism of aortic valve calcification progression. Therefore, this study will examine: 1) the expression of FSTL3 is regulated via Sirt1; 2) FSTL3 bind with proteins to regulated calcification; 3) the mechanism of SOX9-RUNX2 axis was regulated via FSTL3; 4); the mechanism of FSTL3 regulated HIF-1α signaling pathway; 5) in vivo, the aortic valve calcification progress of FSTL3 regulatory mechanisms. Through these studies to explain the mechanisms of aortic valve calcification regulated by FSTL3, which provide a scientific basis and experimental basis for therapeutic intervention in vivo aortic valve calcification.

• The mechanism by which FSTL1 antagonist Aortic valve calcification via DIP2A/CD14

• Calcific aortic valve is one of a variety of risk factors for heart disease, but the pathogenesis is not clear. Now we found that: the expression of FSTL1 is decreased in serum and valve interstitial cells of valve tissues of aortic valve calcification, and negative related with age. Sirt1 and Sirt4 regulated the expression of FSTL1 in valve interstitial cells. Moreover, FSTL1 inhibited the calcification of valve interstitial cells and bind with DIP2A and CD14 as its receptor. The gene chip array showed that FSTL1 regulated SOX9 and RUNX2. These results hint that FSTL1 regulated valvular interstitial cells calcification process via multiple signaling pathways, which is an important mechanism of aortic valve calcification progression. Therefore, this study will examine: 1) calcification process regulated Sirt1/4 expression; 2) the expression of FSTL1 is regulated via Sirt1/4; 3) receptors of FSTL1 effect on aortic valve calcification; 4) the mechanism of SOX9-RUNX2 axis was regulated via FSTL1; 5) in vivo, the aortic valve calcification progress of FSTL1 regulatory mechanisms. Through these studies to explain the mechanisms of aortic valve calcification regulated by FSTL1, which provide a scientific basis and experimental basis for therapeutic intervention in vivo aortic valve calcification.

• FSTL1 regulate the complex of TLR4-CD14-CD209 in macrophages to promote diabetic with atherosclerosis

• The pathological of diabetic with atherosclerosis is more serious,，but the mechanisms is not clear. In the present study, we found that the level of FSTL1 is increased in diabetic with atherosclerosis，and it expressed in the macrophages of diabetic animal plaque. AGEs are positive related to FSTL1 and regulated it expression. FSTL1 promoted lipid accumulation, inflammatory and proliferation. Moreover, FSTL1 bind with TLR4, CD14 and CD209 and increase them forming complex. All of these result hints that FSTL1 regulated the function of macrophages in diabetic with atherosclerosis via TLR4-CD14-CD209 complex. This study is aimed at achieving mechanistic understanding of: 1. RAGE regulate the expression of FATL1. 2. The site of FSTL1 binding with TLR4, CD14 and CD209. 3. FSTL1 regulates the complex of TLR4-CD14-CD209. 4. The complex regulate lipid accumulation and inflammatory in macrophages. 5. The affection of FSTL1 promote the diabetic with atherosclerosis in vivo. This study will demonstrate the exact roles of FSTL1 and macrophages in the pathogenesis of diabetic with atherosclerosis, and aid the design of strategies for clinical treatment of diabetic with atherosclerosis.