Evidence map›Paper›PMID 42698414›Full record

ArticleFrontiers in veterinary science2026

Tumor necrosis factor alpha triggers mitochondrial dysfunction and ROS-driven cytokine amplification in bovine fibroblast-like synoviocytes.

Natalia Andrea Godoy, Jan Gallastegui, Gabriela Velásquez, Stefanie Teuber, Sebastian Brauchi, John Quiroga, Pablo Alarcón, Gabriel Moran, María Angélica Hidalgo, Juan Hancke and 1 more

Abstract read
In one paragraph

Article in Frontiers in veterinary science, 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

11 authors.

Natalia Andrea GodoyLaboratory of Inflammation Pharmacology and Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile.
Jan GallasteguiLaboratory of Cellular Biophysics, Faculty of Medicine, Institute of Physiology, Universidad Austral de Chile, Valdivia, Chile.
Gabriela VelásquezLaboratory of Inflammation Pharmacology and Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile.
Stefanie TeuberLaboratory of Inflammation Pharmacology and Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile.
Sebastian BrauchiLaboratory of Cellular Biophysics, Faculty of Medicine, Institute of Physiology, Universidad Austral de Chile, Valdivia, Chile.
John QuirogaLaboratory of Inflammation Pharmacology and Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile.
Pablo AlarcónLaboratory of Inflammation Pharmacology and Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile.
Gabriel MoranLaboratory of Inflammation Pharmacology and Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile.
María Angélica HidalgoLaboratory of Inflammation Pharmacology and Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile.
Juan HanckeLaboratory of Inflammation Pharmacology and Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile.
Rafael Agustín BurgosLaboratory of Inflammation Pharmacology and Immunometabolism, Faculty of Veterinary Sciences, Institute of Pharmacology and Morphophysiology, Universidad Austral de Chile, Valdivia, Chile.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lameness in dairy cattle, driven by joint inflammation, involves fibroblast-like synoviocytes (FLS) that produce inflammatory mediators and reactive oxygen species (ROS). Tumor necrosis factor alpha (TNF-

Indexed as

bovinefibroblast-like synoviocytesinflammationlamenessmitochondriareactive oxygen speciessynoviocytesTNF-α

Identifiers

PMID42698414
PMCPMC13541457

What OpenQuestion holds

Textmetadata
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.