ArticleFrontiers in immunology2026
An experimental study of early cardiovascular disease and risk factors in a collagen-induced arthritis rat model.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: This study investigated the pathological characteristics and risk factors of early cardiovascular disease (CVD) associated with rheumatoid arthritis (RA) using a collagen-induced arthritis (CIA) rat model. Methods: A total of 120 SPF-grade male SD rats were used. Following CIA induction, echocardiography, histopathology, molecular biology, and lipid profile analysis were employed to dynamically monitor cardiac function, structural changes, and lipid profiles across disease stages (D0-D112) . Results: Sequential progression of cardiac dysfunction: Echocardiography revealed a significant decrease in the mitral valve E/A ratio (MVE/A) starting from D84 (P<0.05), indicating diastolic impairment preceding systolic dysfunction.Myocardial structural abnormalities: The heart-to-body weight ratio (HW/BW) in CIA rats was significantly higher than that in the control group starting from day 84 (*P < 0.01), indicating cardiac hypertrophy. Masson staining revealed progressive myocardial fibrosis with increasing collagen deposition from D56. Abnormal lipid profiles and biomarkers: LDL-C significantly increased from D84 to D112 (*P<0.01), while OX-LDL rose from D98 to D112 (P<0.05); B-type natriuretic peptide (BNP) significantly increased at D112 (*P<0.01), indicating heart failure risk. Negative atherosclerosis findings: No plaque formation was detected in the Oil Red O staining of the aorta and coronary arteries. While macroscopic atherosclerotic plaques were not apparent, microvascular endothelial dysfunction may play a role in the early stages of cardiovascular disease (CVD) . Discussion: Cardiovascular lesions in CIA rats exhibit sequential progression: diastolic dysfunction and myocardial fibrosis emerge first (from D56), followed by systolic dysfunction (from D98), accompanied by lipid metabolism disorders driven by LDL-C and OX-LDL. This model provides an experimental basis for studying the mechanisms of RA-associated cardiac lesions and early intervention.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.