ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Small-molecule LF3 alleviates angiotensin II-induced cardiac dysfunction via attenuating cardiac fibrosis.
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
Cardiac fibrosis significantly contributes to heart failure progression, yet no currently available agents directly target this pathological process. The Wnt/β-catenin signaling pathway has emerged as a key mediator of fibrosis, but its upstream inhibition may have unintended broader effects. In this study, we evaluated the therapeutic potential of LF3, a 4-thioureido-benzenesulfonamide derivative that disrupts the downstream β-catenin/TCF4 interaction, in mitigating cardiac fibrosis and investigated the underlying mechanism. Male mice were subjected to cardiac fibrosis by continuous angiotensin II (Ang II) infusion (1.44 mg/kg/day) for 3 weeks using osmotic minipumps and were treated with LF3 (40 mg/kg/day, intraperitoneal). Mouse cardiac fibroblasts were stimulated with 10
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