• Wenjuan Yang, Yu Zhu, Fuqin Tang, Zhao Jian, and Yingbin Xiao.
• Department of Cardiovascular Surgery, The Second Affiliated Hospital of Army Medical University, Chongqing, China.
• Eur. J. Clin. Invest. 2023 Nov 1; 53 (11): e14051e14051.

ObjectiveHypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) are classified as different diseases but have many similar pathogenic genes and clinical symptoms. Previous research has focused on mutated genes. This study was conducted to identify key molecular mechanisms and explore effective therapeutic targets.MethodsMyocardial tissue was harvested from patients with HCM (n = 3) or DCM (n = 4) during surgery. Hearts donated by healthy traffic accident victims were treated as controls (n = 4). Total proteins were extracted for liquid chromatography-tandem mass spectrometry. Differentially expressed proteins (DEPs) were annotated via GO and KEGG analyses. Selected distinguishing protein abundance was confirmed by western blotting.ResultsCompared with the control group, there were 121 and 76 DEPs in the HCM and DCM groups, respectively. GO terms for these two comparisons are associated with contraction-related components and actin binding. Additionally, the most significantly upregulated and downregulated proteins were periostin and tropomyosin alpha-3 chain in both comparisons. Moreover, when comparing the HCM and DCM groups, we found 60 significant DEPs, and the GO and KEGG terms are related to the calcium signalling pathway. Expression of the calcium regulation-related protein peptidyl-prolyl cis-trans isomerase (FKBP1A) was significantly upregulated in multiple samples.ConclusionHCM and DCM have many mutual pathogenetic pathways. Calcium ion-related processes are among the most significant factors affecting disease development. For HCM and DCM, research on regulating linchpin protein expression or interfering with key calcium-related pathways may be more beneficial than genetic research.© 2023 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.

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