Evidence mapPaperPMID 40465697Full record

ArticlePloS one2025

Gene editing therapy as a therapeutic approach for cardiovascular diseases in animal models: A scoping review.

Quan Duy Vo

Abstract readScoping Review
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Frontiers in immunology · 2026
    Review
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Quan Duy VoDepartment of Cardiovascular Medicine, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama Japan.ORCID https://orcid.org/0000-0001-6100-5452

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiovascular diseases (CVDs) are the leading cause of mortality worldwide, with hereditary genetic factors contributing substantially to disease burden. Current treatments, including lifestyle modifications, pharmacotherapy, and surgical interventions, focus primarily on symptom management but fail to address underlying genetic causes, often resulting in disease progression or recurrence. Gene therapy has emerged as a transformative approach, offering a potential treatment. This review explores its efficacy and safety in animal models, identifying opportunities for future advancements.

methodsThis review investigated studies on gene editing interventions in animal models of CVDs, retrieved from PubMed, ScienceDirect, and Web of Science up to December 2024.

resultA total of 57 studies were included in this review. Mice (86%) were the predominant model, with CRISPR-Cas9 (53%) and AAV vectors (80%) as the most used tools. Key targets included PCSK9 (32%), LDLR (9%), and MYH6/7 (7%), achieving 25-85% editing efficiency in liver/heart tissues. Base editors (ABE/CBE) showed superior safety, with <1% off-targets versus CRISPR-Cas9's 2-5 off-targets per guide. Reported toxicity risks included liver injury (AAVs, 23%) and transient cytokine elevation (LNPs, 14%).

conclusionGene editing therapy shows great potential for treating CVDs, with high efficiency, strong therapeutic outcomes, and favorable safety in animal models. Continued innovation and rigorous evaluation could transform cardiovascular treatment, benefiting patients with untreatable conditions.

Indexed as

Cardiovascular DiseasesGene EditingGenetic TherapyAnimalsCRISPR-Cas SystemsDependovirusDisease Models, AnimalHumansMice

Identifiers

PMID40465697
PMCPMC12136301

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.