Nanowired human cardiac organoid transplantation enables highly efficient and effective recovery of infarcted hearts.
Yu TanRobert C CoyleRyan W BarrsSophia E SilverMei LiDylan J RichardsYiliang LinYuanwen JiangHongjun WangDonald R MenickKristine Y DeLeon-PennellBozhi TianYing MeiPublished in: Science advances (2023)
Human cardiac organoids hold remarkable potential for cardiovascular disease modeling and human pluripotent stem cell-derived cardiomyocyte (hPSC-CM) transplantation. Here, we show cardiac organoids engineered with electrically conductive silicon nanowires (e-SiNWs) significantly enhance the therapeutic efficacy of hPSC-CMs to treat infarcted hearts. We first demonstrated the biocompatibility of e-SiNWs and their capacity to improve cardiac microtissue engraftment in healthy rat myocardium. Nanowired human cardiac organoids were then engineered with hPSC-CMs, nonmyocyte supporting cells, and e-SiNWs. Nonmyocyte supporting cells promoted greater ischemia tolerance of cardiac organoids, and e-SiNWs significantly improved electrical pacing capacity. After transplantation into ischemia/reperfusion-injured rat hearts, nanowired cardiac organoids significantly improved contractile development of engrafted hPSC-CMs, induced potent cardiac functional recovery, and reduced maladaptive left ventricular remodeling. Compared to contemporary studies with an identical injury model, greater functional recovery was achieved with a 20-fold lower dose of hPSC-CMs, revealing therapeutic synergy between conductive nanomaterials and human cardiac organoids for efficient heart repair.
Keyphrases
- left ventricular
- induced pluripotent stem cells
- endothelial cells
- cardiovascular disease
- heart failure
- highly efficient
- type diabetes
- induced apoptosis
- gold nanoparticles
- skeletal muscle
- signaling pathway
- acute myocardial infarction
- mitral valve
- hypertrophic cardiomyopathy
- cell proliferation
- stem cells
- mesenchymal stem cells
- cell death
- cell therapy
- left atrial
- coronary artery disease
- reduced graphene oxide
- cell cycle arrest
- cardiovascular risk factors
- pi k akt