Evidence map›Paper›PMID 40888060›Full record

ReviewDisease models & mechanisms2025

The importance of imperfect pre-clinical models in adolescent idiopathic scoliosis.

Diane S Sepich, Ryan S Gray, Nadav Ahituv, Christina A Gurnett, Jonathan J Rios, Lila Solnica-Krezel, Carol A Wise

Abstract readReview
In one paragraph

Review in Disease models & mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Diane S SepichDepartment of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Ryan S GrayDepartment of Pediatrics, Dell Pediatric Research Institute, University of Texas at Austin Dell Medical School, Austin, TX 78723, USA.
Nadav AhituvDepartment of Bioengineering and Therapeutic Sciences, University of California San Francisco, San Francisco, CA 94158, USA.
Christina A GurnettDepartment of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Jonathan J RiosDepartment of Orthopaedic Surgery, University of Texas Southwestern Medical Center, Dallas, TX 75235, USA.
Lila Solnica-KrezelDepartment of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Carol A WiseDepartment of Orthopaedic Surgery, University of Texas Southwestern Medical Center, Dallas, TX 75235, USA.ORCID 0000-0002-6790-2194

Funding

Non-coding/epigenetic regulationP01HD084387 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI Nadav Ahituv, LILIANNA SOLNICAKREZEL · 2016 to 2026
$14.2M
Towards a Mechanistic Undestanding of Adolscent Idiopathic ScoliosisR01AR072009 · NIAMS · UNIVERSITY OF TEXAS AT AUSTIN · PI Ryan Scott Gray · 2017 to 2026
$3.9M
Eunice Kennedy Shriver National Institute of Child Health and Human Development P01HD084387NIAMS NIH HHS L40 AR079806NIAMS NIH HHS R01 AR072009NICHD NIH HHS P01 HD084387
6 · The paper itself

Abstract

Adolescent idiopathic scoliosis (AIS) is a twisting spinal deformity that occurs in otherwise healthy children at the time of rapid pre-pubescent growth. AIS affects ∼3% of children worldwide and is the most common musculoskeletal diagnosis in pediatric populations, posing a significant physiological, psychosocial and financial burden to patients. Genetic predisposition is a clear and major contributor to AIS, and insights from genomic discoveries are inspiring translational studies ultimately aimed at developing novel diagnostics and therapies. Pre-clinical animal models of AIS are now essential to validate human genetic findings, understand gene-by-environment interactions, and speed etiologic and therapeutic discovery. In this Perspective, we highlight the current status of pre-clinical models of AIS and discuss the challenges posed by the nature of the disorder combined with the limitations of standard approaches. Current research suggests that straightforward genetic targeting of orthologous AIS disease genes in vertebrates may not necessarily yield equivalent physiological phenotypes but nevertheless can be utilized to understand disease mechanisms. Longer-term, appropriately complex models are needed to fully recapitulate the human AIS phenotype arising from genetic, physiological and mechanical interactions.

Indexed as

Disease Models, AnimalScoliosisAdolescentAnimalsGenetic Predisposition to DiseaseHumans

Identifiers

PMID40888060
PMCPMC12452065

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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 OpenQuestion graph.