Evidence map›Paper›PMID 41925863›Full record

ArticleCalcified tissue international2026

Role of Complement Component 9 in Bone Health: Causal Evidence in Humans and Mechanistic Studies in Mice.

Claes Ohlsson, Anna E Törnqvist, Karin H Nilsson, Maria Nethander, Jianyao Wu, Lei Li, Antti Koskela, Sofia Movérare-Skrtic

Abstract read
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In one paragraph

Article in Calcified tissue international, 2026. 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

8 authors.

Claes Ohlsson *Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Vita Stråket 11, 41345, Göteborg, Sweden.
Anna E Törnqvist *Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Vita Stråket 11, 41345, Göteborg, Sweden.
Karin H NilssonDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Vita Stråket 11, 41345, Göteborg, Sweden.
Maria NethanderDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Vita Stråket 11, 41345, Göteborg, Sweden.
Jianyao WuDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Vita Stråket 11, 41345, Göteborg, Sweden.
Lei LiDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Vita Stråket 11, 41345, Göteborg, Sweden.
Antti KoskelaDepartment of Anatomy and Cell Biology, Faculty of Medicine, Institute of Cancer Research and Translational Medicine, University of Oulu, Oulu, Finland.
Sofia Movérare-SkrticDepartment of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Osteoporosis Centre, Centre for Bone and Arthritis Research, Sahlgrenska Academy at University of Gothenburg, Sahlgrenska University Hospital, Vita Stråket 11, 41345, Göteborg, Sweden. sofia.skrtic@gu.se.ORCID http://orcid.org/0000-0001-7982-7438

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement component 9 (C9) is the main pore-forming protein of the terminal membrane attack complex (MAC) in the complement system. The MAC forms a lytic pore in the membrane of target cells and is a key effector of the innate immune system. Excessive complement activation has been implicated in chronic inflammation, which is a well-established risk factor for increased fracture susceptibility. Although other components of the complement system have been linked to bone mass regulation, the role of C9 is unknown. The aim of the present study was to determine the role of C9 for bone health. To determine the role of circulating, mainly liver-derived, C9 in humans, we conducted Mendelian randomization (MR) using a single-SNP instrument and performed genetic colocalization analyses. Genetically predicted higher circulating C9 levels were causally associated with increased risk of forearm fractures and fractures at any bone site. Colocalization analyses supported these findings. Mechanistic studies were performed in mice. As expected, high C9 expression was observed in the liver, while the expression was low in cortical bone and no expression was observed in trabecular bone. Adult female mice with global C9 deletion (C9

Indexed as

Bone and BonesComplement C9AnimalsBone DensityFemaleFractures, BoneHumansMaleMendelian Randomization AnalysisMiceMice, KnockoutComplement C9Bone mineral densityComplement systemFracturesMendelian randomizationMouse model

Identifiers

PMID41925863
PMCPMC13046653

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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.