title: miR-21 in ischemia/reperfusion injury: a double-edged sword?
abstract: MicroRNAs (miRNAs or miRs) are endogenous, small RNA molecules that suppress expression of targeted mRNA. miR-21, one of the most extensively studied miRNAs, is importantly involved in divergent pathophysiological processes relating to ischemia/reperfusion (I/R) injury, such as inflammation and angiogenesis. The role of miR-21 in renal I/R is complex, with both protective and pathological pathways being regulated by miR-21. Preconditioning-induced upregulation of miR-21 contributes to the protection against subsequent renal I/R injury through the targeting of genes such as the proapoptotic gene programmed cell death 4 and interactions between miR-21 and hypoxia-inducible factor. Conversely, long-term elevation of miR-21 may be detrimental to the organ by promoting the development of renal interstitial fibrosis following I/R injury. miR-21 is importantly involved in several pathophysiological processes related to I/R injury including inflammation and angiogenesis as well as the biology of stem cells that could be used to treat I/R injury; however, the effect of miR-21 on these processes in renal I/R injury remains to be studied.
authors.affiliation: Division of Nephrology, Fudan University Zhongshan Hospital, Shanghai, Peoples Republic of China;
authors.forename: Xialian
authors.initials: X
authors.lastname: Xu
authors.affiliation: Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin;
authors.forename: Alison J
authors.initials: AJ
authors.lastname: Kriegel
authors.affiliation: Division of Nephrology, Fudan University Zhongshan Hospital, Shanghai, Peoples Republic of China;
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Jiao
authors.affiliation: Division of Nephrology, Fudan University Zhongshan Hospital, Shanghai, Peoples Republic of China;
authors.forename: Hong
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin;
authors.forename: Xiaowen
authors.initials: X
authors.lastname: Bai
authors.affiliation: Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin;
authors.forename: Jessica
authors.initials: J
authors.lastname: Olson
authors.affiliation: Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin;
authors.forename: Mingyu
authors.initials: M
authors.lastname: Liang
authors.affiliation: Division of Nephrology, Fudan University Zhongshan Hospital, Shanghai, Peoples Republic of China; Institutes of Biomedical Sciences of Shanghai Medical School, Fudan University, Shanghai, Peoples Republic of China; Kidney and Dialysis Institute of Shanghai, Shanghai, Peoples Republic of China; and Kidney and Blood Purification Laboratory of Shanghai, Shanghai, Peoples Republic of China ding.xiaoqiang@zs-hospital.sh.cn.
authors.forename: Xiaoqiang
authors.initials: X
authors.lastname: Ding
mesh_terms: D000818:Animals; D002470:Cell Survival / Q000235:genetics; D005355:Fibrosis / Q000235:genetics; D005786:Gene Expression Regulation; D006801:Humans; D000860:Hypoxia / Q000235:genetics; D007249:Inflammation / Q000235:genetics; D007511:Ischemia / Q000235:genetics*; D019194:Ischemic Preconditioning; D007668:Kidney / Q000098:blood supply; D035683:MicroRNAs / Q000235:genetics / Q000502:physiology*; D018919:Neovascularization, Physiologic / Q000235:genetics; D015427:Reperfusion Injury / Q000235:genetics*; D033581:Stem Cell Transplantation
chemical_list: C524940:MIRN21 microRNA, human; C531950:MIRN21 microRNA, mouse; D035683:MicroRNAs
keywords: angiogenesis; apoptosis; hypoxia; inflammation; microRNA