Evidence map›Paper›PMID 42883727›Full record

ArticleInternational journal of molecular sciences2026

Attenuation of Cardiac Dysfunction in the Collagen-Induced Arthritis Mouse Model Mediated by a Reactive Aldehyde Species Inhibitor.

Wenxian Zhou, Hannah J Johnson, Michael J Duryee, Ali Namvaran, Aradhana Thapa, Cole Blasing, Amy Nelson, Engle E Sharp, Carlos D Hunter, Bryan Hackfort and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 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

19 authors.

Wenxian ZhouDepartment of Internal Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.ORCID 0000-0002-0558-9286
Hannah J JohnsonDepartment of Internal Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.ORCID 0009-0004-2958-6444
Michael J DuryeeDepartment of Internal Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.ORCID 0000-0001-9104-2238
Ali NamvaranDepartment of Pharmacology & Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Aradhana ThapaDepartment of Internal Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Cole BlasingDepartment of Internal Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Amy NelsonDepartment of Internal Medicine, Division of Allergy and Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Engle E SharpDepartment of Internal Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Carlos D HunterDepartment of Internal Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Bryan HackfortDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Bryant R EnglandDepartment of Internal Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Tate M JohnsonDepartment of Internal Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.ORCID 0000-0003-0335-4157
Daniel R AndersonDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of Nebraska Medical Center, Omaha, NE 68198, USA.ORCID 0000-0001-6041-0077
Adam LazorchakAldeyra Therapeutics, Lexington, MA 02421, USA.
Robert G BennettVeterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE 68105, USA.ORCID 0000-0002-0755-6103
Jill A PooleDepartment of Internal Medicine, Division of Allergy and Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.ORCID 0000-0002-6236-2563
Keshore BidaseeDepartment of Pharmacology & Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE 68198, USA.ORCID 0000-0003-4165-8362
Geoffrey M ThieleDepartment of Internal Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.ORCID 0000-0001-5688-8596
Ted R MikulsDepartment of Internal Medicine, Division of Rheumatology & Immunology, University of Nebraska Medical Center, Omaha, NE 68198, USA.ORCID 0000-0002-0897-2272

Funding

Tracking and Evaluation CoreU54GM115458 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI ZHANG, YING · 2016 to 2025
$42.8M
Inflammatory Responses, Fibrotic Mediators, and Comorbidity Burden as Determinants of Myocardial Dysfunction and Heart Failure in Rheumatoid ArthritisK23AR085189 · NIAMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Tate Johnson · 2025 to 2026
$344k
BLRD VA I01 BX003635BLRD VA I01 BX004660BLRD VA I01 BX005687CSRD VA I01 CX002995HSRD VA I01 HX002972NIAMS NIH HHS K23 AR085189NIGMS NIH HHS U54 GM115458NIH HHS 2U54GM115458NIH/NIAMS 5K23AR085189-02NIOSH CDC HHS R01 OH012045United States Department of Defense PR200793United States Department of Veterans Affairs I01BX003635United States Department of Veterans Affairs I01BX004660VA I01 CX002972VA BLR&D I01BX005687VA CSR&D Merit 1I01CX002995
6 · The paper itself

Abstract

Individuals with rheumatoid arthritis (RA) experience increased risk of heart failure. Malondialdehyde-acetaldehyde (MAA) adducts are overexpressed and co-localize with citrullinated (CIT) proteins in RA myocardium. This study investigated whether reactive aldehyde species (RASP) inhibitors prevent MAA formation in vitro and attenuate cardiac dysfunction in a collagen-induced arthritis (CIA) mouse model. Among eight RASP inhibitors screened, ADX-246 demonstrated the greatest inhibition of MAA formation in vitro. Mice with early CIA (week 5) exhibited elevated levels of myocardial MAA adducts, myocardial inflammation, and reduced ejection fraction, but normal cardiac collagen deposition and diastolic function vs. control. By weeks 10-12, mice with chronic CIA demonstrated increased levels of myocardial MAA and CIT adducts, perivascular collagen deposition, and diastolic dysfunction. ADX-246 treatment reduced myocardial levels of MAA and CIT adducts, inflammation, fibrosis, and cardiac dysfunction in CIA. While ADX-246 reduced weight loss and attenuated arthritis severity, it did not reduce serum autoantibody levels or serum markers of inflammation or fibrosis. Indices of diastolic dysfunction significantly correlated with myocardial MAA and CIT levels, collagen deposition, arthritis severity, and weight loss. These findings support the hypothesis that targeting myocardial RASP and MAA formation may represent a novel therapeutic approach for preventing cardiac dysfunction in RA.

Indexed as

AldehydesArthritis, ExperimentalAcetaldehydeAnimalsArthritis, RheumatoidCollagenDisease Models, AnimalMaleMalondialdehydeMiceMice, Inbred DBAMyocardiumAcetaldehydeAldehydesCollagenMalondialdehydecardiac dysfunctioncollagen-induced arthritisheart failuremalondialdehyde acetaldehydereactive aldehyde speciesrheumatoid arthritis

Identifiers

PMID42883727
PMCPMC13665015

What OpenQuestion holds

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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.