Evidence map›Paper›PMID 41942452›Full record

SynthesisNature communications2026

Genetic architecture of lumbar spinal stenosis.

Ville Salo, Juhani Määttä, Jasmin Takala, Anni Heikkilä, FinnGen, Ene Reimann, Reedik Mägi, Estonian Biobank Research Team, Kadri Reis, Abdelrahman G Elhanas and 7 more

Abstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Nature communications, 2026. 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. 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

17 authors.

Ville SaloResearch unit of Population Health, Faculty of Medicine, and Biocenter Oulu, University of Oulu, Oulu, Finland. ville.salo@oulu.fi.ORCID http://orcid.org/0009-0009-0102-7102
Juhani MäättäResearch Unit of Health Sciences and Technology, Faculty of Medicine, University of Oulu, Oulu, Finland.ORCID http://orcid.org/0000-0002-2400-9195
Jasmin TakalaResearch unit of Population Health, Faculty of Medicine, and Biocenter Oulu, University of Oulu, Oulu, Finland.ORCID http://orcid.org/0009-0008-4315-9050
Anni HeikkiläResearch unit of Population Health, Faculty of Medicine, and Biocenter Oulu, University of Oulu, Oulu, Finland.
FinnGen
Ene ReimannEstonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.ORCID http://orcid.org/0000-0002-5410-4433
Reedik MägiEstonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.ORCID http://orcid.org/0000-0002-2964-6011
Estonian Biobank Research Team
Kadri ReisEstonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.
Abdelrahman G ElhanasEstonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.
Anu ReigoEstonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.ORCID http://orcid.org/0009-0008-0226-3396
Priit PaltaEstonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.ORCID http://orcid.org/0000-0001-9320-7008
Tõnu EskoEstonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia.
Ville LeinonenNeurosurgery, Institute of Clinical Medicine, School of Medicine, Faculty of Health Sciences, University of Eastern Finland and Department of Neurosurgery, Kuopio University Hospital, Kuopio, Finland.ORCID http://orcid.org/0000-0002-4282-4687
Jaro KarppinenResearch Unit of Health Sciences and Technology, Faculty of Medicine, University of Oulu, Oulu, Finland.
Eeva Sliz *Research unit of Population Health, Faculty of Medicine, and Biocenter Oulu, University of Oulu, Oulu, Finland.ORCID http://orcid.org/0000-0002-2316-058X
Johannes Kettunen *Research unit of Population Health, Faculty of Medicine, and Biocenter Oulu, University of Oulu, Oulu, Finland.ORCID http://orcid.org/0000-0002-3345-491X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lumbar spinal stenosis (LSS) affects over 100 million people globally, with an increasing incidence due to an ageing population. While LSS is known to be heritable, its genetic basis remains poorly understood. We conduct a genome-wide meta-analysis of LSS in 40,303 cases and 741,469 controls. We identify 73 previously unreported loci in addition to 15 known loci, and highlight spinal degeneration as a key pathogenic mechanism. In 12,784 surgically treated cases, we discover five loci specifically associated with severe disease. Age-of-onset analyses show that most variants influence risk after midlife, but some confer susceptibility as early as age 34. Mendelian randomization further demonstrates causal effects of higher body mass and fat-free mass on LSS risk. Overall, our findings expand knowledge of the genetic background of LSS and inform future translational research.

Indexed as

Genetic Predisposition to DiseaseLumbar VertebraeSpinal StenosisAge of OnsetCase-Control StudiesGenome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single Nucleotide

Identifiers

PMID41942452
PMCPMC13234025

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.