ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Luteolin ameliorates sympathetic stress-induced myocardial injury by inhibiting the VEGFA/VEGFR2 and PI3K/Akt/NF-kappaB signaling pathways.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. 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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Abstract
Sympathetic overactivation is a significant contributor to myocardial injury in cardiovascular disorders. Luteolin, a flavonoid, possesses anti-inflammatory, antioxidant, and anti-apoptotic properties. However, the precise mechanism underlying its ability to alleviate sympathetic overactivation-induced myocardial injury remains incompletely understood. This study aimed to investigate the protective effects of luteolin and its potential mechanisms against myocardial injury induced by sympathetic stress overactivation. The study focused on elucidating the key targets and signaling pathways of luteolin in attenuating sympathetic stress overactivation and myocardial injury. Cardioprotective effects were assessed by examining myocardial inflammation, apoptosis, oxidative stress, and fibrosis at both animal and cellular levels. Additionally, the impact on cardiomyocyte phenotype was evaluated using inhibitors targeting crucial signaling pathways. Molecular docking and dynamics simulations were employed for further validation. Ten core targets associated with luteolin-mediated improvement of sympathetic stress-induced myocardial injury were identified, primarily enriched in the VEGFA/VEGFR2/PI3K/AKT/NF-κB axis. Animal and in vitro studies demonstrated that luteolin attenuated myocardial inflammation, apoptosis, fibrosis, and oxidative stress resulting from sympathetic stress overactivation. Combination with the VEGFR2 inhibitor ALL-993 enhanced the effects of luteolin on AC16 cardiomyocyte phenotype. Molecular docking analyses revealed a high binding affinity of luteolin for VEGFR2, corroborated by molecular dynamics simulations. Luteolin mitigates myocardial injury caused by sympathetic stress overactivation and modulates the VEGFA/VEGFR2/PI3K/AKT/NF-κB axis, providing novel insights into its cardioprotective mechanisms.
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