2022
DOI: 10.1007/s12265-022-10241-0
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The Role of Angiogenesis and Arteriogenesis in Myocardial Infarction and Coronary Revascularization

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Cited by 15 publications
(16 citation statements)
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“…Using serum from healthy subjects and AMI patients to stimulate EPCs of healthy subjects, we found that the serum from AMI patients inhibited the tubule formation of EPCs ( Figure 4 A). When acute myocardial infarction occurs, sudden ischemia occurs, and the body induces a response through angiogenesis and arteriogenesis, thereby improving myocardial perfusion [ 24 ]. During the compensatory response, the body secretes various growth factors.…”
Section: Resultsmentioning
confidence: 99%
“…Using serum from healthy subjects and AMI patients to stimulate EPCs of healthy subjects, we found that the serum from AMI patients inhibited the tubule formation of EPCs ( Figure 4 A). When acute myocardial infarction occurs, sudden ischemia occurs, and the body induces a response through angiogenesis and arteriogenesis, thereby improving myocardial perfusion [ 24 ]. During the compensatory response, the body secretes various growth factors.…”
Section: Resultsmentioning
confidence: 99%
“…A critical role in angiogenesis is played by VEGF, a growth factor mostly induced by hypoxia-inducible factor (HIF) and down-regulated by the von Hippel–Lindau (VHL) suppressor gene. It stimulates angiogenic response in in vivo and in vitro models, bringing survival and migration signaling to endothelial cells (ECs) and inhibiting their apoptosis [ 85 ]. Currently, we know three different receptors of this factor, each one with many different properties.…”
Section: Discussionmentioning
confidence: 99%
“…It is primarily activated by the so-called “canonical ligands”, e.g., its natural activator VEGF-A and co-receptors such as neuropilin (NRP1 and NRP2) and heparan sulfate proteoglycans (HSPGs). Besides these, there are many “non-canonical ligands”, which can stimulate angiogenesis by activating VEGFR2 in mechanical shear stress, such as gremlins, galectins, lactate, and LDLs [ 85 ]. Evidence shows that statins may interfere with VEGF expression.…”
Section: Discussionmentioning
confidence: 99%
“…However, in-stent restenosis (ISR) after stenting of the FP district remains a daunting problem, resulting in a less than 50% patency rate after 3 years [ 4 ]. ISR is believed to be due to neointimal hyperplasia caused by post-PTA endothelial damage [ 5 , 6 ], but similarly to coronary stent disease, other factors are involved such as adherence to antiplatelet therapy [ 7 , 8 ] and specific stent factors [ 9 ]. The incidence of ISR also varies according to the type of stent used: 19–35% at 1 year with a grooved tube nitinol stent, and 14–17% with a twisted-wire nitinol stent [ 4 ].…”
Section: Introductionmentioning
confidence: 99%