一二三四区视频,亚洲少妇熟女色,日本久热无码视频网,欧美国产日韩大尺度,亚洲a视频,久久少妇一区二区,日韩999无码视频,刺激久久久久久久,啊啊啊啊不要啊在线

ChemicalBook >> journal list >> Biochemical and biophysical research communications >>article
Biochemical and biophysical research communications

Biochemical and biophysical research communications

IF: 2.5
Download PDF

Machine Learning and Multi-Omics Integration Reveal TRPV2 as a Central Regulator in Bicuspid Aortic Valve Calcification

Published:21 October 2025 DOI: 10.1016/j.bbrc.2025.152840 PMID: 41151405
Jian Liu , Jin Bai , Faxiong Gao , Chongjun Qi , Chen Tian , Zukai Wu , Cheng Deng

Abstract

Background

Bicuspid aortic valve (BAV), the most common congenital heart defect, is strongly predisposed to early calcification, yet the molecular drivers remain poorly defined. This study aims to identify the functional role of transient receptor potential vanilloid 2 (TRPV2) in valve interstitial cell (VIC) calcification and to explore its upstream and downstream regulatory network.

Methods

Transcriptomic data from calcified BAV tissues (GSE83453, n?=?18) were analyzed using gene set variation analysis, weighted gene co-expression network analysis, and multiple machine learning algorithms. A ceRNA regulatory network was constructed by integrating miRNA–mRNA–lncRNA interactions. Findings were validated in murine VICs using osteogenic induction. TRPV2 function was evaluated by small interfering RNA-mediated knockdown and overexpression assays. Alizarin Red staining, quantitative real-time PCR, Western blot, and dual-luciferase reporter assays were used to assess calcification phenotypes and molecular mechanisms.

Results

Multi-omics integration and machine learning identified TRPV2 as a hub gene associated with calcified BAV tissue. TRPV2 expression is significantly upregulated during osteogenic induction of VICs, while its knockdown reduces calcium nodule formation and suppresses osteogenic markers Runx2 and ALP. Bioinformatics and luciferase assays confirm that miR-3619–5p directly targets the 3′ UTR of TRPV2. TRPV2 overexpression rescued the miR-3619–5p inhibitory effects, restoring calcification phenotypes. A competing endogenous RNA (ceRNA) axis involving TRPV2 is proposed as a novel driver of BAV calcification.

Conclusion

TRPV2 emerges as a potential pro-osteogenic regulator of VIC calcification operating within a ceRNA-linked regulatory axis. These findings nominate TRPV2 and its upstream microRNA interactions as candidate therapeutic targets for mitigating calcific progression in BAV.

Similar articles

尤溪县| 财经| 苏尼特右旗| 炎陵县| 麦盖提县| 长岛县| 内黄县| 南雄市| 东乌珠穆沁旗| 广州市| 玉树县| 达州市| 东兰县| 博罗县| 安远县| 鹤峰县| 河北省| 东莞市| 宁武县| 炎陵县| 乌兰察布市| 宝坻区| 浦江县| 河池市| 贡嘎县| 涿鹿县| 分宜县| 资源县| 县级市| 丰台区| 乌兰察布市| 衡东县| 宜州市| 南阳市| 宁津县| 合江县| 江口县| 华坪县| 攀枝花市| 襄城县| 闽清县|