Abstract

Hypertrophic cardiomyopathy (HCM) represents one of the most common heritable heart diseases. However, the signalling pathways and regulatory networks underlying the pathogenesis of HCM remain largely unknown. Here, we present a strand-specific RNA-seq dataset for both coding and lncRNA profiling in myocardial tissues from 28 HCM patients and 9 healthy donors. This dataset constitutes a valuable resource for the community to examine the dysregulated coding and lncRNA genes in HCM versus normal conditions.

Highlights

  • Background & SummaryHypertrophic cardiomyopathy (HCM) represents one of the most common heart diseases, and a leading cause of sudden death in young people[1,2]

  • HCM is generally regarded as a genetic disorder caused predominately by mutations in eight sarcomere genes, including MYH7, MYBPC3, ACTC1, TPM1, MYL2, MYL3, TNNI3, and TNNT23

  • There is increasing evidence showing that Long non-coding RNAs (lncRNAs) are involved in a variety of biological processes and diseases5,6. lncRNAs have been implicated in pathologically processes of HCM, such as cardiomyocyte disarrangement, myocardial hypertrophy and interstitial fibrosis[7]

Read more

Summary

Introduction

Background & SummaryHypertrophic cardiomyopathy (HCM) represents one of the most common heart diseases (an estimated prevalence of at least 0.2%), and a leading cause of sudden death in young people[1,2]. We still lack a strand-specific RNA-seq dataset for myocardial tissues of HCM patients. We present a strand-specific RNA-seq dataset for both coding and lncRNA profiling in myocardial tissues from 28 HCM patients and 9 healthy donors.

Results
Conclusion
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.