Fucoidan treatment significantly reduced cardiac hypertrophy and fibrosis, as evidenced by decreased heart weight, improved myocardial structure, and reduced markers of oxidative stress, inflammation, and fibrosis, including Gal-3, α-SMA, and collagen I. Furthermore, fucoidan’s modulation of key signaling pathways, such as Keap1/Nrf2 and CD44, highlights its antioxidative and anti-inflammatory properties, which are critical in protecting cardiac tissue under stress [9,10]. Here, ACTA1 is linked to cardiac hypertrophy.