Cardiac cells and mesenchymal stem cells derived extracellular vesicles: a potential therapeutic strategy for myocardial infarction

Figures

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  Figure 1. Biogenesis, composition and uptake of EVs. cells secrete EVs (including exosomes, ectosomes, and apoptotic bodies) and NVEPs (such as supermeres and exomeres) into the extracellular environment. Exosomes are produced via exocytosis, while ectosomes (such as microvesicles and large oncosomes) are formed through budding. Apoptotic bodies are vesicles formed during apoptosis. EVs contain proteins, DNA, RNA, lipids, metabolites, and mitochondria. EVs can also form a corona on their surface. The membrane of EVs predominantly includes GTPase, MHC class I and II molecules, tetraspanins like CD9, CD63, and CD81, as well as various receptors and ligands. EVs are primarily internalized by target cells via receptor-ligand interactions, clathrin-mediated and clathrin-independent endocytosis, pinocytosis, and direct membrane fusion.

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  Figure 2. The EV-mediated cross-talk among various cardiac cells such as CMs, ECs, EPCs, CPCs, CDCs, Mϕ, CFs, CTCs and EPDCs under normal, H2O2, hypoxia or ischemia condition, which are involved in the regulation of angiogenesis, inflammatory response, cell death and myocardial fibrosis.

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  Figure 3. Applications of MSC-EVs in MI. MSC-EVs can be utilized in their original state and enhanced autophagy through preconditioning, gene engineering,membrane modification, encapsulation, hybridization and biomaterial-assisting. EVs can be applied via IM, IV, IC and iPC injection in MI or I/R animal models. MSC-EVs can improve angiogenesis, inflammation, cell death (such as apoptosis, autophgy, pyroptosis, ferroptosis), oxidatve stress and cardiac fibrosis after MI.