Table 3.

Summary of cell-free approaches used in cardiac repair

Alternative strategies		Model	Outcome	Type of disease	References
Exosomes	hESC-derived MSCs	Mouse	Reduced infarct size	Myocardial infarction/ reperfusion injury	[166–168]
	hESCSC-derived cardiovascular progenitor	Mouse	Reduced left ventricular end-systolic and end-diastolic volumes	Chronic heart failure	[169]
	hiPSC-derived cardiovascular progenitor		Improved cardiac function through decreased left ventricular volumes and increased LVEF	Myocardial infarction	[170]
	MSCs	Rat	Reduced apoptosis and the myocardial infarct size	Reperfusion injury	[171]
Modified mRNA	Vascular endothelial growth factor (VEGF)-A	Mouse	Induced vascular regeneration	Myocardial infarction	[172]
		Pig	Improved LVEF, increased angiogenesis, and reduced fibrosis		[173]
		Mouse	Promotes Isl1+ to endothelial cell fate		[174]
	Insulin-like growth factors (IGFs)	Mouse	Promote cardiomyocyte survival and abrogate cell apoptosis post-MI		[175]
Growth factors	VEGF	Pig	Increased myocardial blood flow and improved regional ventricular function	Chronic myocardial ischemia	[176]
	Fibroblast growth factors (FGFs)	Mouse	Induced cardiomyocyte proliferation and division	Ischemic heart disease	[177]
	Neuregulin 1 (NRG-1)	Mouse	Induced cardiomyocyte proliferation and promotes myocardial regeneration	Myocardial infarction	[178]
	Periostin	Rat	Reduced fibrosis and infarct size, and increase angiogenesis	Myocardial infarction	[179]
	Hepatocyte growth factor (HGF)	Rat	Reduced apoptosis of cardiomyocytes and lesion size	Reperfusion injury	[180]
	Platelet-derived growth factor (PDGF)	Rat	Decreased infarct size, decreased cardiomyocyte death, and preserved systolic function	Ischemia/reperfusiomy/myocardial infarction	[181]
	Interleukin (e.g., IL-33, IL-11)	Rat	Reduced cardiomyocyte apoptosis, decreased infarct size and fibrosis, and improved ventricular function	Ischemia/reperfusion	[182]
		Mouse	Reduced fibrosis and increase angiogenesis	Myocardial infarction	[183]