What question did this study set out to answer?

To identify uncharacterized circular RNAs involved in pathological cardiac hypertrophy and define the molecular mechanisms governing their actions.

April 17, 2025Circulation Research

Novel Truncated Peptide Derived From circCDYL Exacerbates Cardiac Hypertrophy

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Authors

MLMengyang Li WDWei Ding XFXinyu Fang

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Overview

Preclinical study reveals that circCDYL-derived peptide tCDYL-100 drives cardiac hypertrophy in mice, highlighting a novel mechanism for therapeutic targeting.

Key Points

To identify uncharacterized circular RNAs involved in pathological cardiac hypertrophy and define the molecular mechanisms governing their actions.
Screened public cardiac circular RNA sequencing data to detect candidates regulated during cardiac hypertrophy.
Conducted in vitro assays using Ang II-treated primary rat cardiomyocytes and in vivo assays using Ang II-infused mice with gain- and loss-of-function genetic modifications.
circCDYL expression was significantly upregulated by Ang II and translated into a truncated 100-amino-acid peptide (tCDYL-100) via prohypertrophic N6-methylation.
tCDYL-100 outcompeted full-length CDYL to bind REST, disrupting the REST-CDYL-EHMT2 corepressor complex and activating pro-hypertrophic genes rhoa and nppb.
Silencing circCDYL prevented Ang II-induced cardiac hypertrophy in mice, whereas direct overexpression of tCDYL-100 alone provoked cardiac hypertrophy.

Cite This Study

Li et al. (2025) studied this question.

synapsesocial.com/papers/6a9d82cb9675ea02512a0e77 https://doi.org/10.1161/circresaha.124.325573

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April 17, 2025Circulation Research

Novel Truncated Peptide Derived From circCDYL Exacerbates Cardiac Hypertrophy

View Full Paper

Ask AI

Bookmark

Authors

MLMengyang Li WDWei Ding XFXinyu Fang

Discussion

Member takes

Overview

Preclinical study reveals that circCDYL-derived peptide tCDYL-100 drives cardiac hypertrophy in mice, highlighting a novel mechanism for therapeutic targeting.

Key Points

To identify uncharacterized circular RNAs involved in pathological cardiac hypertrophy and define the molecular mechanisms governing their actions.
Screened public cardiac circular RNA sequencing data to detect candidates regulated during cardiac hypertrophy.
Conducted in vitro assays using Ang II-treated primary rat cardiomyocytes and in vivo assays using Ang II-infused mice with gain- and loss-of-function genetic modifications.
circCDYL expression was significantly upregulated by Ang II and translated into a truncated 100-amino-acid peptide (tCDYL-100) via prohypertrophic N6-methylation.
tCDYL-100 outcompeted full-length CDYL to bind REST, disrupting the REST-CDYL-EHMT2 corepressor complex and activating pro-hypertrophic genes rhoa and nppb.
Silencing circCDYL prevented Ang II-induced cardiac hypertrophy in mice, whereas direct overexpression of tCDYL-100 alone provoked cardiac hypertrophy.

Cite This Study

Li et al. (2025) studied this question.

synapsesocial.com/papers/6a9d82cb9675ea02512a0e77 https://doi.org/10.1161/circresaha.124.325573

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