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Review
. 2022 Jan;23(1):64.
doi: 10.3892/etm.2021.10986. Epub 2021 Nov 22.

Targeting angiogenesis in myocardial infarction: Novel therapeutics (Review)

Jiejie Li  1 , Yuanyuan Zhao  1 , Wei Zhu  1
Affiliations
Review

Targeting angiogenesis in myocardial infarction: Novel therapeutics (Review)

Jiejie Li et al. Exp Ther Med. 2022 Jan.

Abstract

Acute myocardial infarction (AMI) remains the main cause of mortality worldwide. Despite surgery and medical treatment, the non-regeneration of dead cardiomyocytes and the limited contractile ability of scar tissue can lead to heart failure. Therefore, restoring blood flow in the infarcted area is important for the repair of myocardial injury. The objective of the present review was to summarize the factors influencing angiogenesis after AMI, and to describe the application of angiogenesis for cardiac repair. Collectively, this review may be helpful for relevant studies and to provide insight into future therapeutic applications in clinical practice.

Keywords: acute myocardial infarction; angiogenesis; exosomes; mesenchymal stem cells; vascular endothelial cells.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
Hypoxia stimulation can produce a variety of pro-angiogenic factors. Among them, VEGF can bind to VEGFR2 of endothelial cells via the Notch signaling pathway to downregulate VEGFR2 and secrete sVEGFR1. Moreover, endothelial cells preferentially transform into Tip cells and combine with Stalk cells to form endothelial cells sprouting process. sVEGFR1, soluble VEGFR1; HIF, hypoxia-inducible factor; FGF, fibroblast growth factor receptors; HGF, hepatocyte growth factor.
Figure 2
Figure 2
Main sources and packaging release process of exosomes. Exosomes are mainly derived from MSCs isolated from embryos, adipose tissue and bone marrow. The cell membrane invades to form MVB. Some of the multivesicular bodies are degraded by lysosomes through the Golgi apparatus, and some are fused with the plasma membrane and released outside the cell. Exosomes contain several angiogenic molecules, including miRNAs and proteins, such as VEGF and FGF. MSC, mesenchymal stem cell; miRNA, microRNA; FGF, fibroblast growth factor receptors; MVB, multivesicular bodies.
Figure 3
Figure 3
Application of biomaterials for cardiac repair. MSCs or pro-angiogenic factors can be combined with hydrogels to form biomaterials with improved repair performance, and can be targeted to the site of heart injury by injection, implantation and other ways to form new blood vessels. MSC, mesenchymal stem cell.
Figure 4
Figure 4
Biological factors for the treatment of myocardial infarction. The figure mainly shows two types of biological factors for cardiac repair. The small molecules listed are SDF-1, Annexin V, β-estradiol, irisin, heparan sulfate, dihydrotestosterone and collagenous stromal elements. Catalpa, GeGen-DanShen extract and Ginkgo biloba extract are all Chinese herbal extracts. SDF-1, stromal cell derived factor.
See this image and copyright information in PMC

References

    1. Mehta LS, Beckie TM, DeVon HA, Grines CL, Krumholz HM, Johnson MN, Lindley KJ, Vaccarino V, Wang TY, Watson KE, et al. American Heart Association Cardiovascular Disease in Women and Special Populations Committee of the Council on Clinical Cardiology, Council on Epidemiology and Prevention, Council on Cardiovascular and Stroke Nursing, and Council on Quality of Care and Outcomes Research: Acute Myocardial Infarction in Women: A Scientific Statement From the American Heart Association. Circulation. 2016;133:916–947. doi: 10.1161/CIR.0000000000000351. - DOI - PubMed
    1. Reed GW, Rossi JE, Cannon CP. Acute myocardial infarction. Lancet. 2017;389:197–210. doi: 10.1016/S0140-6736(16)30677-8. - DOI - PubMed
    1. Frangogiannis NG. Cardiac fibrosis: Cell biological mechanisms, molecular pathways and therapeutic opportunities. Mol Aspects Med. 2019;65:70–99. doi: 10.1016/j.mam.2018.07.001. - DOI - PubMed
    1. Mitsos S, Katsanos K, Koletsis E, Kagadis GC, Anastasiou N, Diamantopoulos A, Karnabatidis D, Dougenis D. Therapeutic angiogenesis for myocardial ischemia revisited: Basic biological concepts and focus on latest clinical trials. Angiogenesis. 2012;15:1–22. doi: 10.1007/s10456-011-9240-2. - DOI - PubMed
    1. Lorier G, Touriño C, Kalil RA. Coronary angiogenesis as an endogenous response to myocardial ischemia in adults. Arq Bras Cardiol. 2011;97:e140–e148. doi: 10.1590/s0066-782x2011001500019. - DOI - PubMed