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Related Concept Videos

Animal Mitochondrial Genetics02:59

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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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Updated: Aug 19, 2025

Author Spotlight: Cardiac Cell Transgenesis for Rapid Gene Screening
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Published on: May 24, 2024

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Genome Editing and Myocardial Development.

Sifa Turan1, J Richard Chaillet1,2, Margaret C Stapleton3,4

  • 1Department of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD, USA.

Advances in Experimental Medicine and Biology
|December 1, 2022
PubMed
Summary
This summary is machine-generated.

Genetic editing offers a promising therapeutic approach for congenital heart disease (CHD), a condition with significant genetic causes. Research explores gene editing in mouse models to understand and potentially correct the genetic mutations responsible for CHD.

Keywords:
Cardiovascular diseaseCongenital heart disease (CHD)Heart development

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Area of Science:

  • Cardiovascular Genetics
  • Developmental Biology
  • Gene Editing Technologies

Background:

  • Congenital heart disease (CHD) affects up to 1% of live births, with complex genetic origins involving over 400 genes crucial for myocardial development.
  • Genetic mutations in intricate networks disrupt cardiovascular formation, leading to various heart abnormalities.

Approach:

  • This review examines the anatomical and genetic timelines of myocardial development in humans and mice.
  • It evaluates the potential of genome editing for treating syndromic, nonsyndromic, and familial CHD cases with identifiable mutations.
  • The role of mouse models in replicating human CHD and testing gene correction strategies is discussed.

Key Points:

  • Genome editing technologies present a viable future therapeutic strategy for CHD.
  • Identifiable genetic mutations in various CHD forms indicate potential targets for gene therapy.
  • Mouse models are instrumental in studying CHD pathogenesis and validating gene editing approaches.

Conclusions:

  • CHD's strong genetic basis makes it a prime candidate for gene editing therapies.
  • Advancements in genome editing technology hold promise for correcting causative mutations in CHD.
  • Further research using established mouse models will facilitate the clinical translation of gene editing for CHD treatment.