cardiac fibrosis

Trimethylamine N-oxide (TMAO) is a gut microbiota-dependent metabolite derived from dietary choline, betaine, and carnitine. It induces inflammation by activating the ROS/NLRP3 inflammasome and promotes fibroblast differentiation through the activation of the TGF-β/Smad2 signaling pathway. TMAO is commonly used to induce cardiac fibrosis models.

Trimethylamine N-oxide dihydrate (TMANO dihydrate) is a gut microbiota-dependent metabolite derived from dietary choline and other trimethylamine-containing nutrients. It induces inflammation by activating the ROS NLRP3 inflammasome and promotes fibroblast differentiation and cardiac fibrosis via the TGF-β Smad2 signaling pathway. TMANO dihydrate can be used to establish models of cardiac hypertrophy and cardiac fibrosis.

Angiotensin II is a major biologically active vasoconstrictor peptide that regulates blood pressure by binding to AT1R and AT2R receptors. It stimulates the sympathetic nervous system, promotes aldosterone synthesis, and enhances renal function. Additionally, it induces vascular smooth muscle cell proliferation and increases collagen synthesis, leading to vascular and myocardial hypertrophy and fibrosis. It also promotes apoptosis and endothelial capillary formation. Angiotensin II is commonly used to induce hypertension and cardiac hypertrophy animal models.

Angiotensin II human TFA is a potent vasoconstrictor in the renin-angiotensin system that regulates blood pressure through interactions with AT1R and AT2R receptors. It activates sympathetic nerve activity, promotes aldosterone synthesis and renal function, induces proliferation of vascular smooth muscle cells, and enhances type I and III collagen production in fibroblasts, leading to vascular and myocardial thickening and fibrosis. It also triggers apoptosis and promotes capillary formation, making it suitable for establishing models of cardiac hypertrophy, hypertension, and abdominal aortic aneurysm.

Angiotensin II human acetate is a key vasoconstrictor peptide in the renin-angiotensin system. It regulates blood pressure by binding to AT1R and AT2R receptors, stimulates the sympathetic nervous system, promotes aldosterone synthesis and renal function, induces vascular smooth muscle cell proliferation and collagen synthesis, leading to vascular and myocardial hypertrophy and fibrosis, while also promoting apoptosis and endothelial capillary formation. It is commonly used to induce hypertension and cardiac hypertrophy models.