ArticleFrontiers in pharmacology2025
Xin-Fu-Kang oral liquid improves cardiac function and attenuates miR-223-associated NF-κB/NLRP3 pyroptotic signaling in chronic heart failure.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- MicroRNA-223-3p/NLRP3 axis attenuates LPS-induced sepsis-like myocardial dysfunction by suppressing cardiomyocyte pyroptosis.Molecular biology reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Pyroptotic signaling involving nuclear factor-kappa B (NF-κB) and NOD-like receptor family pyrin domain-containing 3 (NLRP3) has been implicated in chronic heart failure (CHF). Xin-Fu-Kang (XFK) is a nine-herb formula used clinically for CHF with "qi deficiency and blood stasis." Although cardioprotective effects have been reported, it remains unclear whether XFK modulates myocardial pyroptotic signaling via miR-223-dependent regulation of NF-κB. Methods: A CHF model was established by permanent left anterior descending coronary artery (LADCA) ligation in rats, and an Results: LADCA produced marked systolic dysfunction with chamber dilation, increased myocardial IL-1β and IL-18, increased NLRP3, ASC, GSDMD-N, and p65 phosphorylation, and decreased the pro-caspase-1/caspase-1 ratio. XFK improved cardiac function and structural integrity, attenuated fibrosis and cardiomyocyte apoptosis, reduced inflammatory cytokines, and diminished NLRP3 and ASC abundance. In OGD/R-injured H9c2 cells, XFK preserved viability, limited lactate dehydrogenase release, decreased NLRP3, ASC, GSDMD-N, and IL-1β, increased the pro-caspase-1/caspase-1 ratio, and restrained NF-κB activation by reducing p65 phosphorylation and nuclear translocation. Mechanistically, XFK upregulated miR-223, and miR-223 overexpression reproduced the suppression of pyroptosis-related readouts linked to NF-κB/NLRP3 signaling. Inhibition of miR-223 attenuated the protective effects of XFK, supporting the interpretation that XFK-mediated modulation of NF-κB-related inflammatory signaling is at least partly dependent on miR-223. Conclusion: NF-κB-linked NLRP3 pyroptotic signaling represents a prominent feature in the CHF model examined. These findings suggest that XFK exerts protective effects in CHF via miR-223-dependent modulation of NF-κB/NLRP3 pyroptotic signaling, supporting its potential adjunctive strategy to mitigate inflammation-driven cardiac dysfunction.
Indexed as
Identifiers
What Socratic 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 Socratic graph.