ArticleJournal of cardiothoracic surgery2026
Resveratrol ameliorates myocardial injury and inflammatory response and cell apoptosis in Kawasaki disease rats by activating the Nrf2/HO-1 pathway.
Article in Journal of cardiothoracic surgery, 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKawasaki disease (KD) is an acute, self-limiting systemic vasculitis of unknown etiology, which often involves the coronary arteries, leading to severe complications such as myocardial injury (MI). It aimed to explore the mechanism of action of Resveratrol (RES) on MI induced by KD in rats based on the Nrf2/HO-1 pathway.
methodsThirty-six rats were randomly grouped: control, model, RES intervention, Nrf2 inhibitor + RES intervention groups (CG, MG, RG, IRG). The KD rat model was established. After modeling, RES was administered to the RG via intraperitoneal injection, while sterile saline was injected into the CG and MG. Cardiac function, inflammatory factors in myocardial tissue, and related proteins was examined.
resultsAs against the MG, the left ventricular end-diastolic diameter (LVEDd) and left ventricular end-systolic diameter (LVESd) were visibly reduced, while left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were visibly increased in the RG; The levels of inflammatory factors in the RG were visibly decreased but still higher relative to the CG; The relative expression (RE) of Nrf2 and HO-1 in the RG was visibly increased but still lower relative to the CG; In contrast to the MG, the RE of Bcl2 was visibly higher, while the RE of Bax was visibly lower in the RG (P < 0.05); Compared with the RG, the RE of Nrf2 in the nuclear protein of the IRG was significantly decreased to (0.41 ± 0.03) (P < 0.05).
conclusionRES can improve MI and cardiac dysfunction in KD rats by activating the Nrf2/HO-1 pathway, inhibiting inflammatory response and cell apoptosis, providing theoretical and experimental evidence for its application.
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.