MiR-17-92 cluster is a novel regulatory gene of cardiac ischemic/reperfusion injury

Mi Zhou, Junfeng Cai, Yao Liang Tang, Qiang Zhao

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

The miR-17-92 cluster is an important microRNA cluster in the animals. It was mainly investigated as an oncogene in tumors but never studied in cardiovascular disease. On one aspect, miR-17-92 cluster is documented to play anti-apoptotic roles in tumor cells, including hypoxia-induced apoptosis. The families of miR-17, miR-19, and miR-92 promote resistance to apoptosis by directly inhibiting pro-apoptotic protein, and by the two major cell survival signaling pathways-PI3K/AKT, and MAPK/ERK. On the other aspect, the component members of miR-17-92 cluster are high expressed in the hearts of canine and mice, suggesting that there are effect targets of the cluster in the myocardium. So that, we hypothesized that the miR-17-92 cluster may protect the heart by diminishing the apoptosis and alleviating ischemia/reperfusion injury. This may be a new regulating target for patients with myocardial infarction and undergoing cardiac surgery.

Original languageEnglish (US)
Pages (from-to)108-110
Number of pages3
JournalMedical Hypotheses
Volume81
Issue number1
DOIs
StatePublished - Jul 1 2013
Externally publishedYes

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Apoptosis Regulatory Proteins
Regulator Genes
Reperfusion Injury
Apoptosis
MicroRNAs
Phosphatidylinositol 3-Kinases
Oncogenes
Thoracic Surgery
Canidae
Cell Survival
Myocardium
Cardiovascular Diseases
Myocardial Infarction
Neoplasms
Tumor Hypoxia

ASJC Scopus subject areas

  • Medicine(all)

Cite this

MiR-17-92 cluster is a novel regulatory gene of cardiac ischemic/reperfusion injury. / Zhou, Mi; Cai, Junfeng; Tang, Yao Liang; Zhao, Qiang.

In: Medical Hypotheses, Vol. 81, No. 1, 01.07.2013, p. 108-110.

Research output: Contribution to journalArticle

Zhou, Mi ; Cai, Junfeng ; Tang, Yao Liang ; Zhao, Qiang. / MiR-17-92 cluster is a novel regulatory gene of cardiac ischemic/reperfusion injury. In: Medical Hypotheses. 2013 ; Vol. 81, No. 1. pp. 108-110.
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