Mesenchymal stem cell (MSC)-based cardiac patches are envisioned to be a promising treatment option for patients with myocardial infarction. However, their therapeutic efficacy and duration are hampered due to their limited retention on the epicardium. We engineered a scaffold-free MSC sheet with an inherent ability to migrate into the infarcted myocardium, a strategy enabled by actively establishing a sustained intracellular hypoxic environment through the endocytosis of our FDA-approved ferumoxytol. This iron oxide nanoparticle stabilized hypoxia-induced factor-1α, triggering upregulation of the CXC chemokine receptor and subsequent MSC chemotaxis. Thus, MSCs integrated into 2/3 depth of the left ventricular anterior wall in a rat model of acute myocardial infarction and persisted for at least 28 days. This led to spatiotemporal delivery of paracrine factors by MSCs, enhancing cardiac regeneration and function. Ferumoxytol also facilitated the noninvasive MRI tracking of implanted MSCs. Our approach introduces a strategy for mobilizing MSC migration, holding promise for rapid clinical translation in myocardial infarction treatment.
Keyphrases
- left ventricular
- mesenchymal stem cells
- acute myocardial infarction
- heart failure
- hypertrophic cardiomyopathy
- umbilical cord
- mitral valve
- iron oxide
- cardiac resynchronization therapy
- stem cells
- aortic stenosis
- bone marrow
- poor prognosis
- magnetic resonance imaging
- computed tomography
- signaling pathway
- contrast enhanced
- machine learning
- long non coding rna
- optical coherence tomography
- artificial intelligence
- coronary artery disease
- wound healing