What is the clinical evidence from this study?

Study design: Other. Population: Congenital heart disease. Intervention: Deletion of Methyltransferase 14 (M14-KO). Primary outcome: Myocardial dysfunction and embryonic lethality.

October 9, 2025Circulation Research

Abstract NBT101: m6A mRNA Modifications Regulate Metabolic Transition During Cardiogenesis

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Key result

Methyltransferase 14 deletion causes embryonic lethality and myocardial dysfunction by disrupting mitochondrial respiration.

Population

Preclinical models including Methyltransferase 14 knockout in cardiac progenitor cells and a human induced…

Comparison

Deletion of Methyltransferase 14 or suppression… vs Wild-type or unsuppressed controls (implied)

Design

Preclinical

Authors

SLShunyao LeiJohns Hopkins University HGHarshi GangradeJohns Hopkins University SBSheetal BajpayiJohns Hopkins University

Discussion

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Implication

m6A mRNA modifications play a critical role in regulating the metabolic transition during embryonic heart development by modifying YY1 and key electron transport chain genes.

Key Points

Decreased m6A in cardiac progenitors is linked to myocardial dysfunction and several characteristics of congenital heart disease.
Key m6A writer deletion in cardiac cells led to embryonic lethality and reduced cardiomyocyte proliferation.
Single cell RNA-Seq and proteomics revealed critical m6A modifications affecting mitochondrial electron transport chain components.
Findings highlight m6A modification's central role in metabolic transitions during heart development, emphasizing the need for further investigation.

Structured PICO

Population

Preclinical models including Methyltransferase 14 knockout (M14-KO) in cardiac progenitor cells and a human induced pluripotent stem cell (hiPSC)-based model of cardiac development

Intervention

Deletion of Methyltransferase 14 (M14-KO) or suppression of m6A

Comparator

Wild-type or unsuppressed controls (implied)

Outcome

Myocardial dysfunction, embryonic lethality, and morphological changes (ventricular non-compaction, reduced cardiomyocyte proliferation, increased apoptosis)surrogate

m6A mRNA modifications play a critical role in regulating the metabolic transition during embryonic heart development by modifying YY1 and key electron transport chain genes.

Cite This Study

Lei et al. (2025) studied Congenital heart disease. Deletion of Methyltransferase 14 (M14-KO) was evaluated on Myocardial dysfunction and embryonic lethality. Deletion of the m6A writer Methyltransferase 14 in cardiac progenitor cells resulted in myocardial dysfunction and embryonic lethality by disrupting mitochondrial respiration.

synapsesocial.com/papers/68e77f09d1c187e1c108fba3 https://doi.org/10.1161/res.137.suppl_1.nbt101

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Implication

m6A mRNA modifications play a critical role in regulating the metabolic transition during embryonic heart development by modifying YY1 and key electron transport chain genes.

Abstract NBT101: m6A mRNA Modifications Regulate Metabolic Transition During Cardiogenesis

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Abstract NBT101: m6A mRNA Modifications Regulate Metabolic Transition During Cardiogenesis

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider