Aging
Navigate
Submit an Article
Research Paper|Volume 16, Issue 9|pp 8260—8278

HLA-B and TIMP1 as hub genes of the ventricular remodeling caused by hypertension

Gai-Feng Hu1, Ling-Bing Meng2, Jianyi Li3,4, Jiapei Xu3, Hong-Xuan Xu3, De-Ping Liu3,4
  • 1Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, National Clinical Research Center for Cardiovascular Diseases, Chaoyang 100029, Beijing, China
  • 2Department of Cardiology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Changping 102218, Beijing, China
  • 3Department of Cardiology, Beijing Hospital, National Center of Gerontology, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Dong Dan 100730, Beijing, China
  • 4Graduate School of Peking Union Medical College and Chinese Academy of Medical Sciences, Dongcheng 100730, Beijing, China
* Equal contribution
Received: January 8, 2024Accepted: April 10, 2024Published: May 9, 2024
https://doi.org/10.18632/aging.205816

Copyright: © 2024 Hu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Rationale: Myocardial fibrosis is an important pathological change that occurs during ventricular remodeling in patients with hypertension and is an important pathophysiological basis of cardiovascular disease. However, the molecular mechanism underlying this ventricular remodeling is unclear.

Methods: Bioinformatics analysis identified HLA-B and TIMP1 as hub genes in the process of myocardial fibrosis. Expression and correlation analyses of significant hub genes with ventricular remodeling were performed. Weighted gene co-expression network analysis (WGCNA) was performed to verify the role of HLA-B. ceRNA network was constructed to identify the candidate molecule drugs. Receiver operating characteristic (ROC) curves were analyzed.

Results: RT-qPCR was performed to verify the roles of HLA-B and TIMP1 in seven control individuals with hypertension and seven patients with hypertension and ventricular remodeling. The WGCNA showed that HLA-B was in the brown module and the correlation coefficient between HLA-B and ventricular remodeling was 0.67. Based on univariate logistic proportional regression analysis, HLA-B influences ventricular remodeling (P<0.05). RT-qPCR showed that the relative expression levels of HLA-B and TIMP1 were significantly higher in HLVR samples compared with their expression in the control group.

Conclusions: HLA-B and TIMP1 might provide novel research targets for the diagnosis and treatment of HLVR.