Evidence map›Paper›PMID 32195011›Full record

ReviewBone research2020

The cartilage matrisome in adolescent idiopathic scoliosis.

Carol A Wise, Diane Sepich, Aki Ushiki, Anas M Khanshour, Yared H Kidane, Nadja Makki, Christina A Gurnett, Ryan S Gray, Jonathan J Rios, Nadav Ahituv and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Bone research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
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

40 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Deletion of aJOR spine · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Genetic interaction betweenbioRxiv : the preprint server for biology · 2026
    Article
  12. Genetic interaction betweenResearch square · 2026
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Rare missense variants inJournal of medical genetics · 2025
    Article
  18. Article
  19. Review
  20. 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

11 authors at 5 institutions in 1 country.

Carol A Wise1Center for Pediatric Bone Biology and Translational Research, Texas Scottish Rite Hospital for Children, 2222 Welborn St., Dallas, TX 75219 USA.ORCID 0000-0002-6790-2194
Diane Sepich5Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110 USA.
Aki Ushiki6Department of Bioengineering and Therapeutic Sciences, University of California San Francisco, San Francisco, CA 94158 USA.
Anas M Khanshour1Center for Pediatric Bone Biology and Translational Research, Texas Scottish Rite Hospital for Children, 2222 Welborn St., Dallas, TX 75219 USA.
Yared H Kidane1Center for Pediatric Bone Biology and Translational Research, Texas Scottish Rite Hospital for Children, 2222 Welborn St., Dallas, TX 75219 USA.
Nadja Makki8Department of Anatomy and Cell Biology, University of Florida, College of Medicine, Gainesville, FL 32610 USA.
Christina A Gurnett9Departments of Neurology, Washington University School of Medicine, St Louis, MO 63110 USA.
Ryan S Gray12Department of Pediatrics, Dell Pediatric Research Institute, University of Texas at Austin Dell Medical School, Austin, TX 78723 USA.
Jonathan J Rios1Center for Pediatric Bone Biology and Translational Research, Texas Scottish Rite Hospital for Children, 2222 Welborn St., Dallas, TX 75219 USA.
Nadav Ahituv6Department of Bioengineering and Therapeutic Sciences, University of California San Francisco, San Francisco, CA 94158 USA.
Lila Solnica-Krezel5Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110 USA.
Texas Scottish Rite Hospital for Children · USWashington University in St. Louis · USUniversity of California, San Francisco · USDell Children's Medical Center of Central Texas · USUniversity of Florida · US

Funding

Non-coding/epigenetic regulationP01HD084387 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI Nadav Ahituv, LILIANNA SOLNICAKREZEL · 2016 to 2026
$14.2M
Genetic Risk Factors for Severe ScoliosisR01AR067715 · NIAMS · WASHINGTON UNIVERSITY · PI DOBBS, MATTHEW BARRETT, GURNETT, CHRISTINA · 2015 to 2024
$6.0M
Towards a Mechanistic Undestanding of Adolscent Idiopathic ScoliosisR01AR072009 · NIAMS · UNIVERSITY OF TEXAS AT AUSTIN · PI Ryan Scott Gray · 2017 to 2026
$3.9M
NIAMS NIH HHS R01 AR067715NIAMS NIH HHS R01 AR072009NICHD NIH HHS P01 HD084387
6 · The paper itself

Abstract

The human spinal column is a dynamic, segmented, bony, and cartilaginous structure that protects the neurologic system and simultaneously provides balance and flexibility. Children with developmental disorders that affect the patterning or shape of the spine can be at risk of neurologic and other physiologic dysfunctions. The most common developmental disorder of the spine is scoliosis, a lateral deformity in the shape of the spinal column. Scoliosis may be part of the clinical spectrum that is observed in many developmental disorders, but typically presents as an isolated symptom in otherwise healthy adolescent children. Adolescent idiopathic scoliosis (AIS) has defied understanding in part due to its genetic complexity. Breakthroughs have come from recent genome-wide association studies (GWAS) and next generation sequencing (NGS) of human AIS cohorts, as well as investigations of animal models. These studies have identified genetic associations with determinants of cartilage biogenesis and development of the intervertebral disc (IVD). Current evidence suggests that a fraction of AIS cases may arise from variation in factors involved in the structural integrity and homeostasis of the cartilaginous extracellular matrix (ECM). Here, we review the development of the spine and spinal cartilages, the composition of the cartilage ECM, the so-called "matrisome" and its functions, and the players involved in the genetic architecture of AIS. We also propose a molecular model by which the cartilage matrisome of the IVD contributes to AIS susceptibility.

Indexed as

Bone quality and biomechanicsPathogenesis

Identifiers

PMID32195011
PMCPMC7062733
OpenAlexW3010327772

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.