Evidence map›Paper›PMID 34526398›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

Annexin A1 attenuates cardiac diastolic dysfunction in mice with inflammatory arthritis.

Jianmin Chen, Lucy V Norling, Jose Garrido Mesa, Marina De Paula Silva, Sophie E Burton, Chris Reutelingsperger, Mauro Perretti, Dianne Cooper

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

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  5. Inflammation and Resolution in Obesity-Related Cardiovascular Disease.International journal of molecular sciences · 2026
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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 at 2 institutions in 2 countries.

Jianmin ChenWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, United Kingdom; jianmin.chen@qmul.ac.uk d.cooper@qmul.ac.uk.ORCID 0000-0003-0098-0857
Lucy V NorlingWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, United Kingdom.ORCID 0000-0001-5316-9115
Jose Garrido MesaWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, United Kingdom.ORCID 0000-0001-6420-9055
Marina De Paula SilvaWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Sophie E BurtonWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, United Kingdom.
Chris ReutelingspergerDepartment of Biochemistry, Cardiovascular Research Institute, Maastricht University, Maastricht 6229HX, The Netherlands.ORCID 0000-0002-2334-9403
Mauro PerrettiWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, United Kingdom.ORCID 0000-0003-2068-3331
Dianne CooperWilliam Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, United Kingdom; jianmin.chen@qmul.ac.uk d.cooper@qmul.ac.uk.ORCID 0000-0002-5553-9447
Queen Mary University of London · GBMaastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) carries a twofold increased incidence of heart failure with preserved ejection fraction, accompanied by diastolic dysfunction, which can lead to death. The causes of diastolic dysfunction are unknown, and there are currently no well-characterized animal models for studying these mechanisms. Current medications for RA do not have marked beneficial cardio-protective effects. K/BxN F1 progeny and KRN control mice were analyzed over time for arthritis development, monitoring left ventricular diastolic and systolic function using echocardiography. Excised hearts were analyzed by flow cytometry, qPCR, and histology. In pharmacological experiments, K/BxN F1 mice were treated with human recombinant AnxA1 (hrAnxA1, 1 μg/mouse) or vehicle daily. K/BxN F1 mice exhibited fully developed arthritis with normal cardiac function at 4 wk; however, by week 8, all mice displayed left ventricular diastolic dysfunction with preserved ejection fraction. This dysfunction was associated with cardiac hypertrophy, myocardial inflammation and fibrosis, and inflammatory markers. Daily treatment of K/BxN F1 mice with hrAnxA1 from weeks 4 to 8 halted progression of the diastolic dysfunction. The treatment reduced cardiac transcripts of proinflammatory cytokines and profibrotic markers. At the cellular level, hrAnxA1 decreased activated T cells and increased MHC II

Indexed as

AnimalsAnnexin A1Arthritis, RheumatoidCardiomyopathiesDiastoleDisease Models, AnimalHeartHeart DiseasesHeart FailureHeart Failure, DiastolicHeart VentriclesMaleMiceMice, Inbred C57BLMice, Inbred NODMyocardiumAnnexin A1annexin A1, mouseannexin A1arthritiscardiomyopathydiastolic dysfunctionHFpEF

Identifiers

PMID34526398
PMCPMC8463875
OpenAlexW3199730097

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.