The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Inhibition of MicroRNA-92a Protects Against Ischemia/Reperfusion Injury in a Large-Animal Model
Open accessAbstract
Background—: MicroRNAs (miRs) are small noncoding RNAs that posttranscriptionally control gene expression. Small-animal studies suggest that miRs might offer novel therapeutic targets in cardiovascular diseases such as cardioprotection of murine hearts after myocardial infarction via miR-92a inhibitors. Because the functional benefits of miR-92a inhibitors in larger preclinical models are not known, we assessed the therapeutic efficacy of miR-92a inhibition in a porcine model of ischemia and reperfusion. Methods and Results—: Pigs (n=5 per group) underwent percutaneous ischemia/reperfusion (60 min/72 h or 7 days, respectively). Locked nucleic acid–modified antisense miR-92a (LNA-92a) was applied either regionally (antegrade or retrograde) with a catheter or systemically (intravenously). LNA-92a significantly ( P <0.01) reduced miR-92a expression in the infarct zone regardless of the application venue. However, catheter-based delivery, but not intravenous infusion, of LNA-92a significantly ( P <0.05) reduced the infarct size compared with control LNA–treated pigs, which correlated with an improved ejection fraction and left ventricular end-diastolic pressure ( P <0.05). Histochemistry revealed that LNA-92a increased capillary density but decreased leukocyte influx and cardiac cell death. Complete loss of miR-92a in mice attenuated the infarct-related myocardial dysfunction to a larger extent than cardiomyocyte-specific miR-92a deletion. In vitro, LNA-92a protected against hypoxia/reoxygenation–induced cardiomyocyte cell death. Conclusions—: Regional LNA-92a delivery reduces miR-92a levels and infarct size and postischemic loss of function. LNA-92a exerts cell-protective, proangiogenic, and anti-inflammatory effects. miR-92a inhibition might be a novel therapeutic tool to preserve cardiac function after ischemia.
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Cites
MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts
Thum, T., Gross, C., Fiedler, J., Fischer, T., Kissler, S., Bussen, M., Galuppo, P., Just, S., Rottbauer, W., Frantz, S., et al. (2008) · Nature · doi:10.1038/nature07511 · Cited by 2,349
Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis
van Rooij, E., Sutherland, L. B., Thatcher, J. E., DiMaio, J. M., Naseem, R. H., Marshall, W. S., Hill, J. A., & Olson, E. N. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0805038105 · Cited by 1,844
Self-citationLNA-mediated microRNA silencing in non-human primates
Elmén, J., Lindow, M., Schütz, S., Lawrence, M., Petri, A., Obad, S., Lindholm, M., Hedtjärn, M., Hansen, H. F., Berger, U., et al. (2008) · Nature · doi:10.1038/nature06783 · Cited by 1,589
MicroRNA-92a Controls Angiogenesis and Functional Recovery of Ischemic Tissues in Mice
Bonauer, A., Carmona, G., Iwasaki, M., Mione, M., Koyanagi, M., Fischer, A., Burchfield, J., Fox, H., Doebele, C., Ohtani, K., et al. (2009) · Science · doi:10.1126/science.1174381 · Cited by 1,215
Self-citationRegulation of the Inflammatory Response in Cardiac Repair
Frangogiannis, N. G. (2012) · Circulation Research · doi:10.1161/circresaha.111.243162 · Cited by 1,194
Pervasive roles of microRNAs in cardiovascular biology
Small, E. M., & Olson, E. N. (2011) · Nature · doi:10.1038/nature09783 · Cited by 1,180
Inhibition of miR-15 Protects Against Cardiac Ischemic Injury
Hullinger, T. G., Montgomery, R. L., Seto, A. G., Dickinson, B. A., Semus, H. M., Lynch, J. M., Dalby, C. M., Robinson, K., Stack, C., Latimer, P. A., et al. (2012) · Circulation Research · doi:10.1161/circresaha.111.244442 · Cited by 501
Self-citationDoebele, C., Bonauer, A., Fischer, A., Scholz, A., Reiss, Y., Urbich, C., Hofmann, W.-K., Zeiher, A. M., & Dimmeler, S. (2010) · Blood · doi:10.1182/blood-2010-01-264812 · Cited by 362
Self-citationStress-dependent cardiac remodeling occurs in the absence of microRNA-21 in mice
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Self-citationmiR-24 inhibits apoptosis and represses Bim in mouse cardiomyocytes
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Cited by
miRNAS in cardiovascular diseases: potential biomarkers, therapeutic targets and challenges
Zhou, S.-S., Jin, J.-P., Wang, J.-Q., Zhang, Z.-G., Freedman, J. H., Zheng, Y., & Cai, L. (2018) · Acta Pharmacologica Sinica · doi:10.1038/aps.2018.30 · Cited by 675
Development of microRNA therapeutics is coming of age
van Rooij, E., & Kauppinen, S. (2014) · EMBO Molecular Medicine · doi:10.15252/emmm.201100899 · Cited by 625
Self-citationNoncoding RNAs regulate NF-κB signaling to modulate blood vessel inflammation
Cheng, H. S., Njock, M.-S., Khyzha, N., Dang, L. T., & Fish, J. E. (2014) · Frontiers in Genetics · doi:10.3389/fgene.2014.00422 · Cited by 69
Song, Y.-S., Joo, H.-W., Park, I.-H., Shen, G.-Y., Lee, Y., Shin, J. H., Kim, H., & Kim, K.-S. (2017) · PLOS ONE · doi:10.1371/journal.pone.0179972 · Cited by 53
Cell type–specific microRNA therapies for myocardial infarction
Liu, B., Wang, B., Zhang, X., Lock, R., Nash, T., & Vunjak-Novakovic, G. (2021) · Science Translational Medicine · doi:10.1126/scitranslmed.abd0914 · Cited by 53
Metadata
- Authors
- Hinkel, R., Penzkofer, D., Zühlke, S., Fischer, A., Husada, W., Xu, Q.-F., Baloch, E., van Rooij, E., Zeiher, A. M., Kupatt, C., & Dimmeler, S.
- Venue
- Circulation
- Published
- 2013-09-03
- Volume
- 128
- Issue
- 10
- Pages
- 1066-1075
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2117903449
- Cited by
- 317
- References
- 24
- FWCI
- 21.12
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Inhibition of MicroRNA-92a Protects Against Ischemia/Reperfusion Injury in a Large-Animal Model. https://app.cochat.ai/papers/10.1161/circulationaha.113.001904
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- Hinkel, R., Penzkofer, D., Zühlke, S., Fischer, A., Husada, W., Xu, Q.-F., Baloch, E., van Rooij, E., Zeiher, A. M., Kupatt, C., & Dimmeler, S. (2013). Inhibition of MicroRNA-92a Protects Against Ischemia/Reperfusion Injury in a Large-Animal Model. Circulation. https://doi.org/10.1161/circulationaha.113.001904
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