Whether Letrozole could reduce the incidence of early ovary hyperstimulation syndrome after assisted reproductive technology? A systematic review and meta-analysis
REPRODUCTIVE HEALTH
Authors: Zhao, Jing; Xu, Bin; Huang, Xi; Yan, Yi; Li, Yanping
Abstract
Background Letrozole can significantly decrease the estrogen level, and has been administrated to prevent the incidence of early ovary hyperstimulation syndrome (OHSS). However, the effect of Letrozole on prevention of OHSS reached to controversial conclusions. The present meta-analysis aim to examine whether Letrozole could reduce the incidence of early OHSS after assisted reproductive technology (ART). Methods An exhaustive electronic literature search was conducted on MEDLINE, Google Scholar, CNKI and WANFANG MED ONLINE, from inception until May 2018. We include clinical trials that examined the effect of Letrozole on the prevention of early OHSS. The main outcome measures were the incidence of total early OHSS, mild early OHSS, moderate early OHSS, and severe early OHSS. Results Eight studies included in the review. Of these, five publications evaluated the effect of Letrozolel on the prevention of total, mild, moderate, and severe OHSS, respectively. The results indicated that there was a significantly decreased incidence of total OHSS with Letrozole compared with control group, and there were no significantly differences in the incidence of mild, moderate, and severe OHSS between study group with Letrozole and control group. Eight studies reported the incidence of moderate + severe OHSS. We found a significant decrease in incidence of moderate + severe OHSS in high-risk women with Letrozole. Conclusions Letrozole has no beneficial effect on the prevention of mild, moderate, and severe OHSS, individually; Letrozole should not be considered as the first-line treatment for prevention of OHSS. Further cohort studies are required to explore the effect of Letrozole on the prevention of OHSS. Plain English Summary This study aimed to examine whether Letrozole could reduce the incidence of early OHSS after assisted reproductive technology (ART). A meta-analysis including 8 studies was conducted. There were no significantly differences in the incidence of mild, moderate, and severe OHSS between study group with Letrozole and control group. Letrozole has no beneficial effect on the prevention of mild, moderate, and severe OHSS, individually.
Knockdown of estrogen-related receptor alpha inhibits valve interstitial cell calcification in vitro by regulating heme oxygenase 1
FASEB JOURNAL
Authors: Hu, Wangxing; Wu, Rongrong; Gao, Chenyang; Liu, Feng; Zeng, Zhiru; Zhu, Qifeng; Chen, Jinyong; Cheng, Si; Yu, Kaixiang; Qian, Yi; Zhao, Jing; Zhong, Shuhan; Li, Qingju; Wang, Lihan; Liu, Xianbao; Wang, Jian'an
Abstract
Calcific aortic valve disease (CAVD) is the most common valvular heart disease in adults. The cellular mechanisms of CAVD are still unknown, but accumulating evidence has revealed that osteogenic differentiation of human valve interstitial cells (hVICs) plays an important role in CAVD. Thus, we aimed to investigate the function of estrogen-related receptor alpha (ERR alpha) in the osteogenic differentiation of hVICs. We found that the level of ERR alpha was significantly increased in CAVD samples compared to normal controls. In addition, ERR alpha was significantly upregulated during hVIC osteogenic differentiation in vitro. Gain- and loss-of-function experiments were performed to identify the function of ERR alpha in hVIC calcification in vitro. Inhibition of endogenous ERR alpha attenuated hVIC calcification, whereas overexpression of ERR alpha in hVICs promoted this process. RNA sequencing results suggested that heme oxygenase-1 (Hmox1) was a downstream target of ERR alpha, which was further confirmed by western blotting. Additionally, we also found that downregulation of Hmox1 by shHmox1 efficiently reversed the inhibition of calcification induced by ERR alpha shRNA in hVICs. ChIP-qPCR and luciferase assays indicated that Hmox1 was negatively regulated by ERR alpha. We found that overexpression of Hmox1 or its substrates significantly inhibited hVIC calcification in vitro. In conclusion, we found that knockdown of ERR alpha can inhibit hVIC calcification through upregulating Hmox1 and that ERR alpha and Hmox1 are potential targets for the treatment of CAVD.