ArticleiScience2024
Transcriptome analysis of human hypertrophic cardiomyopathy reveals inhibited cardiac development pathways in children.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Decoding the Histomorphological and Multi-Omic Characteristics of Melanotic Schwannoma.Current medical science · 2026Article
- Nonmuscle α-Actinin-4 Couples Sarcomere Function to Cardiac Remodeling.Circulation research · 2026Article
- Exploring transcriptomic signatures in sudden unexplained death (SUD) cases.International journal of legal medicine · 2025Article
- Nanodomain cAMP signaling in cardiac pathophysiology: potential for developing targeted therapeutic interventions.Physiological reviews · 2025Review
- Transcriptomic and genetic profiling in a spontaneous non-human primate model of hypertrophic cardiomyopathy and sudden cardiac death.Scientific reports · 2024Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epidemiological, etiological, and clinical characteristics vary greatly between pediatric (P-HCM) and adult (A-HCM) hypertrophic cardiomyopathy (HCM) patients, and the understanding of the heterogeneous pathogenesis mechanisms is insufficient to date. In this study, we aimed to comprehensively assess the respective transcriptome signatures and uncover the essential differences in gene expression patterns among A-HCM and P-HCM. The transcriptome data of adults were collected from public data (GSE89714), and novel pediatric data were first obtained by RNA sequencing from 14 P-HCM and 9 infantile donor heart samples. Our study demonstrates the common signatures of myofilament or protein synthesis and calcium ion regulation pathways in HCM. Mitochondrial function is specifically dysregulated in A-HCM, whereas the inhibition of cardiac developing networks typifies P-HCM. These findings not only distinguish the transcriptome characteristics in children and adults with HCM but also reveal the potential mechanism of the higher incidence of septal defects in P-HCM patients.
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Registered trials
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