ArticleFrontiers in cardiovascular medicine2025
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Article in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
8 authors.
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Abstract
Background: Myocardial fibrosis (MF) is a prevalent pathological condition associated with various heart diseases, such as heart failure and arrhythmias, which disrupt electrical signals and reduce pumping efficiency. This research explored the therapeutic effects and potential mechanisms of Methods: Results: LVFP significantly inhibited fibrosis biomarker such as hydroxyproline (HYP) and decreased myocardial fibrosis level as shown by heart weight to tibia length (HW/TL) measurement when compared to ISO-treated mice. Additionally, it increased ejection fraction (EF) and fractional shortening (FS) levels. LVFP showed decreased collagen levels compared to the ISO-treated mice by histological quantification of cardiac fibrosis. Based on the monosaccharide structures of LVFP, 413 targets were identified, with 67 associated with MF. Analysis indicated that the 9 hub genes (AKT1, HSP90AA1, SRC, GSK3β, VEGFR2, RHOA, ENO1, PKM, and IL-2) play roles in MF treatment by participating in signaling pathways related to prostate cancer, lipid and atherosclerosis, and insulin resistance. Molecular docking results showed that LVFP exhibited strong binding potential to VEGFR2 (-8.65 kcal/mol), AKT1 (-7.36 kcal/mol) and GSK3β (-7.68 kcal/mol). Conclusion: LVFP shows promise as a therapeutic agent for MF, primarily through the regulation of various signaling pathways and targets. These findings provide novel insights for the treatment of MF utilizing LVFP.
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