Evidence map›Paper›PMID 40338959›Full record

ArticlePloS one2025

Gene delivery of AGAT and GAMT boosts creatine levels in creatine transporter deficiency patient fibroblasts.

Chloe Wells, Jon Sorgenfrei, Sadie L Johnson, Devin Albertson, Jared Rutter, Steven Andrew Baker

Abstract read
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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

6 authors.

Chloe WellsDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.
Jon SorgenfreiDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.ORCID 0009-0008-8566-9323
Sadie L JohnsonDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.
Devin AlbertsonDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.ORCID 0009-0001-3744-8728
Jared RutterDepartment of Biochemistry, University of Utah, Salt Lake City, Utah, United States of America.
Steven Andrew BakerDepartment of Pathology, University of Utah, Salt Lake City, Utah, United States of America.ORCID 0000-0002-8421-7519

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Creatine is a critical metabolite used to buffer cellular energy demands in highly energetic tissues such as the brain and muscle. Genetic defects in endogenous creatine synthesis or transport across cellular membranes lead to a common set of phenotypes referred to as Cerebral Creatine Deficiency Syndrome (CCDS). The most common form of CCDS is Creatine Transporter 1 (CT1) Deficiency (CTD). It accounts for ~ 70% of cases and results from loss-of-function mutations in the X-linked gene SLC6A8. Affected individuals suffer from intellectual disability, autistic-like behaviors, and epilepsy. There are currently no effective therapies for this disorder, but gene therapy has emerged as a potential approach. The two enzymes which comprise the endogenous creatine synthetic pathway (AGAT and GAMT) are selectively expressed by specific cell types throughout the body. However, after synthesized, creatine uptake relies on the protein product of SLC6A8, CT1, to transport creatine into target cell types. We hypothesized that gene delivery of GATM (encoding AGAT) and GAMT into end-user cell types would bypass the need for CT1, allowing for intracellular synthesis of creatine. We tested this strategy in two human cell types: HEK293T cells and primary fibroblasts. Co-delivery of GATM and GAMT increased internal creatine concentrations by 7.6-fold in HEK293T cells and 12.3-fold in healthy control fibroblasts. We then employed this approach to primary fibroblasts from patients with CTD. This resulted in an up to 11.6-fold increase in intracellular creatine concentrations, far exceeding the intracellular concentration of creatine in healthy control fibroblasts. Importantly, overexpression of AGAT and GAMT resulted in proper targeting of these enzymes to their natural cellular compartment and did not impair the growth of patient fibroblasts. These findings establish gene therapy with GATM and GAMT as a potential strategy for patients with CTD.

Indexed as

AmidinotransferasesBrain Diseases, Metabolic, InbornCreatineFibroblastsGuanidinoacetate N-MethyltransferaseMembrane Transport ProteinsNerve Tissue ProteinsPlasma Membrane Neurotransmitter Transport ProteinsX-Linked Intellectual DisabilityGenetic TherapyGene Transfer TechniquesHumansAmidinotransferasesCreatinecreatine transporterGAMT protein, humanGuanidinoacetate N-MethyltransferaseMembrane Transport ProteinsNerve Tissue ProteinsPlasma Membrane Neurotransmitter Transport ProteinsSLC6A8 protein, human

Identifiers

PMID40338959
PMCPMC12061113

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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 OpenQuestion graph.