The DOI matches its Crossref record; 12 of the 12 references it cites were found in a registry or an index.
Dynamin-Related Protein 1–Mediated Mitochondrial Mitotic Fission Permits Hyperproliferation of Vascular Smooth Muscle Cells and Offers a Novel Therapeutic Target in Pulmonary Hypertension
Open accessAbstract
Rationale: Pulmonary arterial hypertension (PAH) is a lethal syndrome characterized by pulmonary vascular obstruction caused, in part, by pulmonary artery smooth muscle cell (PASMC) hyperproliferation. Mitochondrial fragmentation and normoxic activation of hypoxia-inducible factor-1α (HIF-1α) have been observed in PAH PASMCs; however, their relationship and relevance to the development of PAH are unknown. Dynamin-related protein-1 (DRP1) is a GTPase that, when activated by kinases that phosphorylate serine 616, causes mitochondrial fission. It is, however, unknown whether mitochondrial fission is a prerequisite for proliferation. Objective: We hypothesize that DRP1 activation is responsible for increased mitochondrial fission in PAH PASMCs and that DRP1 inhibition may slow proliferation and have therapeutic potential. Methods and Results: Experiments were conducted using human control and PAH lungs (n=5) and PASMCs in culture. Parallel experiments were performed in rat lung sections and PASMCs and in rodent PAH models induced by the HIF-1α activator, cobalt, chronic hypoxia, and monocrotaline. HIF-1α activation in human PAH leads to mitochondrial fission by cyclin B1/CDK1–dependent phosphorylation of DRP1 at serine 616. In normal PASMCs, HIF-1α activation by CoCl 2 or desferrioxamine causes DRP1-mediated fission. HIF-1α inhibition reduces DRP1 activation, prevents fission, and reduces PASMC proliferation. Both the DRP1 inhibitor Mdivi-1 and siDRP1 prevent mitotic fission and arrest PAH PASMCs at the G2/M interphase. Mdivi-1 is antiproliferative in human PAH PASMCs and in rodent models. Mdivi-1 improves exercise capacity, right ventricular function, and hemodynamics in experimental PAH. Conclusions: DRP-1–mediated mitotic fission is a cell-cycle checkpoint that can be therapeutically targeted in hyperproliferative disorders such as PAH.
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Cites
Kim, J.-W., Tchernyshyov, I., Semenza, G. L., & Dang, C. V. (2006) · Cell Metabolism · doi:10.1016/j.cmet.2006.02.002 · Cited by 3,905
Mitochondrial fusion and fission in cell life and death
Westermann, B. (2010) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3013 · Cited by 2,002
Disruption of Fusion Results in Mitochondrial Heterogeneity and Dysfunction
Chen, H., Chomyn, A., & Chan, D. C. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m503062200 · Cited by 1,376
The anaphase promoting complex/cyclosome: a machine designed to destroy
Peters, J.-M. (2006) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm1988 · Cited by 1,315
Mitotic phosphorylation of dynamin-related GTPase Drp1 participates in mitochondrial fission.
Taguchi, N., Ishihara, N., Jofuku, A., Oka, T., & Mihara, K. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m607279200 · Cited by 1,226
Cassidy-Stone, A., Chipuk, J. E., Ingerman, E., Song, C., Yoo, C., Kuwana, T., Kurth, M. J., Shaw, J. T., Hinshaw, J. E., Green, D. R., et al. (2008) · Developmental Cell · doi:10.1016/j.devcel.2007.11.019 · Cited by 1,200
Inhibiting Mitochondrial Fission Protects the Heart Against Ischemia/Reperfusion Injury
Ong, S.-B., Subrayan, S., Lim, S. Y., Yellon, D. M., Davidson, S. M., & Hausenloy, D. J. (2010) · Circulation · doi:10.1161/circulationaha.109.906610 · Cited by 986
Karbowski, M., Lee, Y.-J., Gaume, B., Jeong, S.-Y., Frank, S., Nechushtan, A., Santel, A., Fuller, M., Smith, C. L., & Youle, R. J. (2002) · The Journal of Cell Biology · doi:10.1083/jcb.200209124 · Cited by 846
Wang, G., & Semenza, G. (1993) · Blood · doi:10.1182/blood.v82.12.3610.3610 · Cited by 766
Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models
Brooks, C., Wei, Q., Cho, S.-G., & Dong, Z. (2009) · Journal of Clinical Investigation · doi:10.1172/jci37829 · Cited by 735
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Relevant Issues in the Pathology and Pathobiology of Pulmonary Hypertension
Tuder, R. M., Archer, S. L., Dorfmüller, P., Erzurum, S. C., Guignabert, C., Michelakis, E., Rabinovitch, M., Schermuly, R., Stenmark, K. R., & Morrell, N. W. (2013) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2013.10.025 · Cited by 585
Self-citationSIRT3 Deacetylates and Activates OPA1 To Regulate Mitochondrial Dynamics during Stress
Samant, S. A., Zhang, H. J., Hong, Z., Pillai, V. B., Sundaresan, N. R., Wolfgeher, D., Archer, S. L., Chan, D. C., & Gupta, M. P. (2014) · Molecular and Cellular Biology · doi:10.1128/mcb.01483-13 · Cited by 446
Self-citation
Metadata
- Authors
- Marsboom, G., Toth, P. T., Ryan, J. J., Hong, Z., Wu, X., Fang, Y.-H., Thenappan, T., Piao, L., Zhang, H. J., Pogoriler, J., Chen, Y., Morrow, E., Weir, E. K., Rehman, J., & Archer, S. L.
- Venue
- Circulation Research
- Published
- 2012-05-25
- Volume
- 110
- Issue
- 11
- Pages
- 1484-1497
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2121580924
- Cited by
- 463
- References
- 12
- FWCI
- 18.74
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Marsboom, G., Toth, P. T., Ryan, J. J., Hong, Z., Wu, X., Fang, Y.-H., Thenappan, T., Piao, L., Zhang, H. J., Pogoriler, J., Chen, Y., Morrow, E., Weir, E. K., Rehman, J., & Archer, S. L. (2012). Dynamin-Related Protein 1–Mediated Mitochondrial Mitotic Fission Permits Hyperproliferation of Vascular Smooth Muscle Cells and Offers a Novel Therapeutic Target in Pulmonary Hypertension. Circulation Research. https://doi.org/10.1161/circresaha.111.263848
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