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Vascul Pharmacol. 2016 Jan;76:1-10. doi: 10.1016/j.vph.2015.08.005. Epub 2015 Aug 5.

Apelinergic system in endothelial cells and its role in angiogenesis in myocardial ischemia.

Author information

1
Integrated Center of Cellular Therapy and Regenerative Medicine, International Clinical Research Center, St. Anne's University Hospital, Brno, Czech Republic.
2
Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA; Mayo Clinic College of Medicine, Mayo Clinic, Rochester, MN 55905, USA.
3
Division of Engineering, Mayo Clinic, Rochester, MN 55905, USA; Mayo Clinic College of Medicine, Mayo Clinic, Rochester, MN 55905, USA.
4
Department of Internal Medicine - Cardiology, Palacky University, Olomouc, Czech Republic; Regional Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, Brno, Czech Republic. Electronic address: martin.klabusay@mou.cz.

Abstract

Apelin is a peptide known to have a vital role in cardiovascular diseases. It has been proven to induce proliferation and tube formation in endothelial cells, stabilise contacts between endothelial cells, and mediate pericyte recruitment. Since apelin level is reduced early after myocardial infarction, a supportive therapy with apelin is being investigated for its beneficial effect on blood vessel formation. It is becoming apparent, however, that the final effect of apelin often depends on stimuli the cell receives and the cross-talk with other molecules inside the cell. Hence, understanding the apelin pathway potentially can help us to improve angiogenic therapy. This review summarises recent knowledge regarding molecules involved in apelin signalling while focusing on their roles in angiogenesis within the ischemic environment after myocardial infarction.

KEYWORDS:

Angiogenesis; Apelin; Apelin-12 (PubChem CID: 479167); Apelin-13 (PubChem CID: 71433878); Apelin-36 (PubChem CID: 16130451); Endothelial cells; Myocardial infarction; Signalling pathways; [Pyr1]-apelin-13 (PubChem CID: 25078060)

PMID:
26254105
DOI:
10.1016/j.vph.2015.08.005
[Indexed for MEDLINE]

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