MicroRNAs as Potential Pharmaco-targets in Ischemia-Reperfusion Injury Compounded by Diabetes.


Journal

Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052

Informations de publication

Date de publication:
12 02 2019
Historique:
received: 09 01 2019
revised: 06 02 2019
accepted: 10 02 2019
entrez: 15 2 2019
pubmed: 15 2 2019
medline: 15 2 2019
Statut: epublish

Résumé

Ischemia-Reperfusion (I/R) injury is the tissue damage that results from re-oxygenation of ischemic tissues. There are many players that contribute to I/R injury. One of these factors is the family of microRNAs (miRNAs), which are currently being heavily studied. This review aims to critically summarize the latest papers that attributed roles of certain miRNAs in I/R injury, particularly in diabetic conditions and dissect their potential as novel pharmacologic targets in the treatment and management of diabetes. PubMed was searched for publications containing microRNA and I/R, in the absence or presence of diabetes. All papers that provided sufficient evidence linking miRNA with I/R, especially in the context of diabetes, were selected. Several miRNAs are found to be either pro-apoptotic, as in the case of miR-34a, miR-144, miR-155, and miR-200, or anti-apoptotic, as in the case of miR-210, miR-21, and miR-146a. Here, we further dissect the evidence that shows diverse cell-context dependent effects of these miRNAs, particularly in cardiomyocytes, endothelial, or leukocytes. We also provide insight into cases where the possibility of having two miRNAs working together to intensify a given response is noted. This review arrives at the conclusion that the utilization of miRNAs as translational agents or pharmaco-targets in treating I/R injury in diabetic patients is promising and becoming increasingly clearer.

Sections du résumé

BACKGROUND
Ischemia-Reperfusion (I/R) injury is the tissue damage that results from re-oxygenation of ischemic tissues. There are many players that contribute to I/R injury. One of these factors is the family of microRNAs (miRNAs), which are currently being heavily studied. This review aims to critically summarize the latest papers that attributed roles of certain miRNAs in I/R injury, particularly in diabetic conditions and dissect their potential as novel pharmacologic targets in the treatment and management of diabetes.
METHODS
PubMed was searched for publications containing microRNA and I/R, in the absence or presence of diabetes. All papers that provided sufficient evidence linking miRNA with I/R, especially in the context of diabetes, were selected. Several miRNAs are found to be either pro-apoptotic, as in the case of miR-34a, miR-144, miR-155, and miR-200, or anti-apoptotic, as in the case of miR-210, miR-21, and miR-146a. Here, we further dissect the evidence that shows diverse cell-context dependent effects of these miRNAs, particularly in cardiomyocytes, endothelial, or leukocytes. We also provide insight into cases where the possibility of having two miRNAs working together to intensify a given response is noted.
CONCLUSIONS
This review arrives at the conclusion that the utilization of miRNAs as translational agents or pharmaco-targets in treating I/R injury in diabetic patients is promising and becoming increasingly clearer.

Identifiants

pubmed: 30759843
pii: cells8020152
doi: 10.3390/cells8020152
pmc: PMC6406262
pii:
doi:

Substances chimiques

MicroRNAs 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Déclaration de conflit d'intérêts

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

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Auteurs

Hassan Dehaini (H)

Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. had29@mail.aub.edu.

Hussein Awada (H)

Department of Biology, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. hma86@mail.aub.edu.

Ahmed El-Yazbi (A)

Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. ae88@aub.edu.lb.
Department of Pharmacology and Toxicology, Alexandria University, Alexandria P.O. Box 21521, El-Mesallah, Egypt. ae88@aub.edu.lb.

Fouad A Zouein (FA)

Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. fz15@aub.edu.lb.

Khodr Issa (K)

Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. ki12@aub.edu.lb.

Assaad A Eid (AA)

Department of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. ae49@aub.edu.lb.

Maryam Ibrahim (M)

Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. mki04@mail.aub.edu.

Adnan Badran (A)

Department of Nutrition, University of Petra, Amman P.O Box 961343 Amman, Jordan. abadran@uop.edu.jo.

Elias Baydoun (E)

Department of Biology, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. eliasbay@aub.edu.lb.

Gianfranco Pintus (G)

Department of Biomedical Sciences, College of Health Sciences, Qatar University, Doha P.O. Box 2713, Qatar. gpintus@qu.edu.qa.
Biomedical Research Center, Qatar University, Doha P.O. Box 2713, Qatar. gpintus@qu.edu.qa.

Ali H Eid (AH)

Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. ae81@aub.edu.lb.
Department of Biomedical Sciences, College of Health Sciences, Qatar University, Doha P.O. Box 2713, Qatar. ae81@aub.edu.lb.

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