Home CONTACT General Physiology and Biophysics 2023 General Physiology and Biophysics Vol.42, No.4, p. 361–372, 2023

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

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General Physiology and Biophysics Vol.42, No.4, p. 361–372, 2023

Title: Weighted gene coexpression network analysis reveals negative regulation of hypertrophic cardiomyopathy by carboxylesterase 1 and cathepsin C
Author: Ye Kuang, Jia Wang, Yulin Dong, Yun Cheng, Hongyan Li, Yong Ji, Hui Gao , Xianghong Cao
Abstract: Hypertrophic cardiomyopathy (HCM) is a primary cardiomyopathy characterized by hypertrophic cardiomyocytes. It is one of the leading causes of sudden death in adolescents. However, the molecular mechanism of HCM is not clear. In our study, ribonucleic acid (RNA) sequence data of myocardial tissue in HCM patients were extracted from the Gene Expression Omnibus (GEO) database (GSE130036) and analyzed by weighted gene coexpression network analysis (WGCNA). A total of 31 coexpression modules were identified. The coexpression black module significantly correlated with maximum left ventricular wall thickness (Maxi LVWT). We screened the differentially expressed mRNAs between normal tissues and HCM tissues using the dplyr and tidyr packages in R3.6.2. The genes in the black module and differentially expressed genes were further intersected. We found that the expression of carboxylesterase 1 (CES1) and cathepsin C (CTSC) was downregulated in HCM tissues and negatively correlated with Maxi LVWT. We further verified the expression of CES1 and CTSC was downregulated in HCM clinical blood and negatively correlated with Maxi LVWT. Finally, we demonstrated that overexpression of CTSC and CES1 could alleviate HCM in an HCM cell model. In summary, the study suggests that CES1 and CTSC negatively regulate the development of HCM and have potential as therapeutic and diagnostic targets for HCM.
Keywords: WGCNA — Carboxylesterase 1 — Cathepsin C — Hypertrophic cardiomyopathy — Maximum left ventricular wall thickness
Published online: 03-Jul-2023
Year: 2023, Volume: 42, Issue: 4 Page From: 361, Page To: 372
doi:10.4149/gpb_2023009


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