August 6, 2025Open Access

A genetically engineered vertebrate animal model of NAA15-related heart disease uncovers myocardial growth, contractility, and mitochondrial defects

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Authors

WPWarlen Pereira Piedade OWOlivia Weeks AAAlexander A. Akerberg

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Overview

Genetically engineered zebrafish model uncovers myocardial defects and contractility issues linked to naa15 mutations, suggesting implications for congenital heart disease.

Key Points

Double homozygous naa15-deficient zebrafish exhibited reduced cardiac size and contractility, indicating severe defects in heart development.
Restoration of wild-type naa15a partially improved heart contractility, showing the gene's role in cardiac function.
Quantitative proteomics revealed mitochondrial abnormalities associated with naa15 disruption in cardiac tissues.
The findings highlight the contribution of naa15 mutations to congenital heart disease, enhancing understanding of its pathogenesis.

Cite This Study

Piedade et al. (2025) studied this question.

synapsesocial.com/papers/689a0fa0e6551bb0af8d1902 https://doi.org/10.1101/2025.08.04.668548

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August 6, 2025Open Access

A genetically engineered vertebrate animal model of NAA15-related heart disease uncovers myocardial growth, contractility, and mitochondrial defects

View Full Paper

Ask AI

Bookmark

Authors

WPWarlen Pereira Piedade OWOlivia Weeks AAAlexander A. Akerberg

Discussion

Member takes

Overview

Genetically engineered zebrafish model uncovers myocardial defects and contractility issues linked to naa15 mutations, suggesting implications for congenital heart disease.

Key Points

Double homozygous naa15-deficient zebrafish exhibited reduced cardiac size and contractility, indicating severe defects in heart development.
Restoration of wild-type naa15a partially improved heart contractility, showing the gene's role in cardiac function.
Quantitative proteomics revealed mitochondrial abnormalities associated with naa15 disruption in cardiac tissues.
The findings highlight the contribution of naa15 mutations to congenital heart disease, enhancing understanding of its pathogenesis.

Cite This Study

Piedade et al. (2025) studied this question.

synapsesocial.com/papers/689a0fa0e6551bb0af8d1902 https://doi.org/10.1101/2025.08.04.668548

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