Evidence map›Paper›PMID 41953844›Full record

ArticleJournal of orthopaedic translation2026

Hydrogen sulfide generated by cystathionine gamma lyase inhibits lysyl oxidase and protects against calcific tendinopathy.

Elodie Faure, Ilaria Bernabei, Driss Ehirchiou, Philipp Michel, Daniel Kronenberg, Thomas Pap, Giuseppe Cirino, Richard Stange, Nathalie Busso, Sonia Nasi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of orthopaedic translation, 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

10 authors.

Elodie FaureService of Rheumatology, Department of Musculoskeletal Medicine, Lausanne University Hospital, Switzerland.
Ilaria BernabeiService of Rheumatology, Department of Musculoskeletal Medicine, Lausanne University Hospital, Switzerland.
Driss EhirchiouService of Rheumatology, Department of Musculoskeletal Medicine, Lausanne University Hospital, Switzerland.
Philipp MichelTrauma, Hand and Reconstructive Surgery, University Hospital Münster, Germany.
Daniel KronenbergDepartment of Regenerative Musculoskeletal Medicine, Institute for Musculoskeletal Medicine, University Hospital Münster, Germany.
Thomas PapDepartment of Molecular Medicine, Institute for Musculoskeletal Medicine, University of Münster, Germany.
Giuseppe CirinoDepartment of Pharmacy, University of Naples Federico II, Naples, Italy.
Richard StangeDepartment of Regenerative Musculoskeletal Medicine, Institute for Musculoskeletal Medicine, University Hospital Münster, Germany.
Nathalie BussoService of Rheumatology, Department of Musculoskeletal Medicine, Lausanne University Hospital, Switzerland.
Sonia NasiService of Rheumatology, Department of Musculoskeletal Medicine, Lausanne University Hospital, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background/objective: Increased lysyl oxidase (LOX) activity favors pathologic cartilage and vessel calcification. LOX promotes disease through enhanced collagen cross-linking, inflammation, reactive oxygen species (ROS) production, cell trans-differentiation, and fibrosis. This study investigates the therapeutic potential of cystathionine gamma lyase (CSE)-generated hydrogen sulfide (H Methods: Human shoulder supraspinatus tendons with varying degrees of CT were analyzed using Alizarin Red staining and LOX and CSE immunohistochemistry to evaluate the correlation between CSE and LOX/calcification. Mechanistic studies were performed using wild-type (WT) and CSE knockout murine tenocytes cultured in calcification-inducing medium with or without H Results: An inverse correlation between CSE levels and LOX/calcification was observed in human tendons and in the surgery-induced CT murine model. In murine tenocytes and in the aging murine model, CSE deficiency led to increased LOX expression, enhanced calcification, and reduced tendon biomechanical integrity.Transcriptomic analysis confirmed the negative association between CSE and LOX in murine CT. Mechanistically, H Conclusion: Dysregulated LOX activity is a key driver of calcific tendinopathy. CSE-generated H The translational potential of this article: This study identifies LOX as a therapeutic target in CT and supports H

Indexed as

Cystathionine-gamma-lyaseHydrogen sulfideLysyl oxidaseLysyl oxidase inhibitionPathologic calcificationTendinopathy

Identifiers

PMID41953844
PMCPMC13053855

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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.