Evidence map›Paper›PMID 41377389›Full record

ReviewAnnals of medicine and surgery (2012)2025

CRISPR-Cas9 gene editing for hereditary angioedema: current treatments and emerging therapies.

Laiba Jalal, Muskan Asim Taimuri, Anusha Sumbal, Areeba Ikram, Tehreem Ali, Ayesha Khan, Safa Alam, Umulkhairah Onyioiza Arama, Hermann Yokolo

Abstract readReview
In one paragraph

Review in Annals of medicine and surgery (2012), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

9 authors.

Laiba JalalDepartment of Internal Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0009-0003-4147-3138
Muskan Asim TaimuriDepartment of Internal Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0000-0001-9457-6411
Anusha SumbalDepartment of Internal Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0000-0003-0685-9767
Areeba IkramDepartment of Internal Medicine, Dow University of Health Sciences, Karachi, Pakistan.ORCID https://orcid.org/0000-0002-0028-7641
Tehreem AliDepartment of Internal Medicine, Dow University of Health Sciences, Karachi, Pakistan.
Ayesha KhanDepartment of Internal Medicine, Dow University of Health Sciences, Karachi, Pakistan.
Safa AlamDepartment of Internal Medicine, Karachi Medical and Dental College, Karachi, Pakistan.ORCID https://orcid.org/0009-0001-8028-9961
Umulkhairah Onyioiza AramaDepartment of Internal Medicine, College of Medical Sciences, Ahmadu Bello University, Kaduna State, Nigeria.ORCID https://orcid.org/0000-0002-1693-9819
Hermann YokoloDepartment of Research, Medical Research Circle (MedReC), Goma, DR Congo.ORCID https://orcid.org/0009-0002-8347-7236

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hereditary angioedema (HAE) is a rare autosomal dominant disorder marked by episodic, non-urticarial swelling due to C1 esterase inhibitor (C1-INH) deficiency or dysfunction, leading to excessive bradykinin-mediated vascular permeability. While current treatments focus on symptomatic control using C1-INH replacement or kallikrein inhibitors, they require frequent administration and do not address the underlying genetic defect. CRISPR-Cas9 gene-editing technologies, particularly the investigational therapy NTLA-2002, offer a transformative approach by targeting the

Indexed as

CRISPRCRISPR-Cas9 gene therapyemerging therapieshereditary angioedema

Identifiers

PMID41377389
PMCPMC12688763

What OpenQuestion holds

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Registered trials

None linked

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 OpenQuestion graph.