Hassan Dehaini1, Hussein Awada2, Ahmed El-Yazbi3,4, Fouad A Zouein5, Khodr Issa6, Assaad A Eid7, Maryam Ibrahim8, Adnan Badran9, Elias Baydoun10, Gianfranco Pintus11,12, Ali H Eid13,14. 1. Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. had29@mail.aub.edu. 2. Department of Biology, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. hma86@mail.aub.edu. 3. Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. ae88@aub.edu.lb. 4. Department of Pharmacology and Toxicology, Alexandria University, Alexandria P.O. Box 21521, El-Mesallah, Egypt. ae88@aub.edu.lb. 5. Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. fz15@aub.edu.lb. 6. Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. ki12@aub.edu.lb. 7. 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. 8. Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. mki04@mail.aub.edu. 9. Department of Nutrition, University of Petra, Amman P.O Box 961343 Amman, Jordan. abadran@uop.edu.jo. 10. Department of Biology, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. eliasbay@aub.edu.lb. 11. Department of Biomedical Sciences, College of Health Sciences, Qatar University, Doha P.O. Box 2713, Qatar. gpintus@qu.edu.qa. 12. Biomedical Research Center, Qatar University, Doha P.O. Box 2713, Qatar. gpintus@qu.edu.qa. 13. Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon. ae81@aub.edu.lb. 14. Department of Biomedical Sciences, College of Health Sciences, Qatar University, Doha P.O. Box 2713, Qatar. ae81@aub.edu.lb.
Abstract
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.
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 diabeticpatients is promising and becoming increasingly clearer.
Entities:
Keywords:
apoptosis; diabetes; ischemia-reperfusion injury; microRNA; pharmaco-targets; reactive oxygen species
Authors: Rong Rong Liu; Jun Li; Jiu Yu Gong; Fang Kuang; Jia Yun Liu; Yu Si Zhang; Qian Li Ma; Chao Jun Song; Agnieszka D Truax; Feng Gao; Kun Yang; Bo Quan Jin; Li Hua Chen Journal: Am J Physiol Heart Circ Physiol Date: 2015-09-14 Impact factor: 4.733
Authors: Huina Zhang; Jian Liu; Dan Qu; Li Wang; Jiang-Yun Luo; Chi Wai Lau; Pingsheng Liu; Zhen Gao; George L Tipoe; Hung Kay Lee; Chi Fai Ng; Ronald Ching Wan Ma; Xiaoqiang Yao; Yu Huang Journal: Diabetes Date: 2016-01-28 Impact factor: 9.461
Authors: Bradley W Ellis; George Ronan; Xiang Ren; Gokhan Bahcecioglu; Satyajyoti Senapati; David Anderson; Eileen Handberg; Keith L March; Hsueh-Chia Chang; Pinar Zorlutuna Journal: Small Date: 2022-06-07 Impact factor: 15.153
Authors: Bradley W Ellis; Dmitry O Traktuev; Stephanie Merfeld-Clauss; Uryan Isik Can; Meijing Wang; Ray Bergeron; Pinar Zorlutuna; Keith L March Journal: Stem Cells Date: 2020-12-23 Impact factor: 6.277