Key result
LOS@SMONs-CHP/MMP2 nanoparticles improve murine systolic function vs free losartan by suppressing cardiac fibroblast activation.
Why the study?
Drug delivery to injured myocardium in myocardial fibrosis is hindered by the dynamic cardiac microenvironment and a lack of lesion-specific targeting.
Does LOS@SMONs-CHP/MMP2 improve cardiac systolic function and reduce fibrosis in a murine model of ISO-induced myocardial fibrosis compared to free losartan?
Does LOS@SMONs-CHP/MMP2 improve cardiac systolic function and reduce fibrosis in a murine model of ISO-induced myocardial fibrosis compared to free losartan?
A dual-targeted nanoparticle delivery system for losartan significantly improved cardiac systolic function and reduced fibrosis in a murine model compared to free losartan, offering a promising platform for treating cardiac fibrosis.
Dual-targeted nanoparticles enable preclinical myocardial fibrosis drug delivery; leaves open clinical translation and outcome impact.
Myocardial fibrosis (MF) drives heart failure and arrhythmias, yet drug delivery to injured myocardium is hindered by the dynamic cardiac microenvironment and lack of lesion-specific targeting. Here, we developed a dual-targeted, soft mesoporous organosilica nanoparticles (SMONs) system, which were co-functionalized with a cardiac homing peptide (CHP) and an anti-matrix metalloproteinase 2 antibody (Ab-MMP 2) for the delivery of losartan (LOS). LOS@SMONs-CHP/MMP2 exhibited excellent deformability and outstanding cellular uptake capability. In a murine model of isoproterenol (ISO)-induced myocardial fibrosis, LOS@SMONs-CHP/MMP2 exhibited significantly increased accumulation of fibrosis. In vitro treatment with these nanoparticles potently suppressed cardiac fibroblast activation, proliferation and migration, and markedly reduced collagen deposition and expression of fibrotic markers in vivo. Consequently, cardiac systolic function was substantially improved, outperforming free losartan. Comprehensive biosafety evaluations confirmed minimal cytotoxicity and no acute organ toxicity. This study offering a promising and translatable nano platform for the treatment of cardiac fibrosis.
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Yang et al. (2026) studied Myocardial fibrosis. LOS@SMONs-CHP/MMP2 (losartan-loaded dual-targeted soft mesoporous organosilica nanoparticles) vs. Free losartan was evaluated on Cardiac fibroblast activation, proliferation, migration, collagen deposition, and cardiac systolic function. LOS@SMONs-CHP/MMP2 nanoparticles potently suppressed cardiac fibroblast activation and collagen deposition, substantially improving cardiac systolic function compared to free losartan in a murine model.
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