The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Mitochondrial division/mitophagy inhibitor (Mdivi) Ameliorates Pressure Overload Induced Heart Failure
Open accessAbstract
BACKGROUND: We have previously reported the role of anti-angiogenic factors in inducing the transition from compensatory cardiac hypertrophy to heart failure and the significance of MMP-9 and TIMP-3 in promoting this process during pressure overload hemodynamic stress. Several studies reported the evidence of cardiac autophagy, involving removal of cellular organelles like mitochondria (mitophagy), peroxisomes etc., in the pathogenesis of heart failure. However, little is known regarding the therapeutic role of mitochondrial division inhibitor (Mdivi) in the pressure overload induced heart failure. We hypothesize that treatment with mitochondrial division inhibitor (Mdivi) inhibits abnormal mitophagy in a pressure overload heart and thus ameliorates heart failure condition. MATERIALS AND METHODS: To verify this, ascending aortic banding was done in wild type mice to create pressure overload induced heart failure and then treated with Mdivi and compared with vehicle treated controls. RESULTS: Expression of MMP-2, vascular endothelial growth factor, CD31, was increased, while expression of anti angiogenic factors like endostatin and angiostatin along with MMP-9, TIMP-3 was reduced in Mdivi treated AB 8 weeks mice compared to vehicle treated controls. Expression of mitophagy markers like LC3 and p62 was decreased in Mdivi treated mice compared to controls. Cardiac functional status assessed by echocardiography showed improvement and there is also a decrease in the deposition of fibrosis in Mdivi treated mice compared to controls. CONCLUSION: Above results suggest that Mdivi inhibits the abnormal cardiac mitophagy response during sustained pressure overload stress and propose the novel therapeutic role of Mdivi in ameliorating heart failure.
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Cites
Heart Disease and Stroke Statistics—2010 Update: A Report From the American Heart Association
WRITING GROUP MEMBERS, Lloyd-Jones, D., Adams, R. J., Brown, T. M., Carnethon, M., Dai, S., De Simone, G., Ferguson, T. B., Ford, E., Furie, K., et al. (2010) · Circulation · doi:10.1161/circulationaha.109.192667 · Cited by 5,700
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 · cited 1×
“Though mitochondrial dynamics involve both fission and fusion mechanisms, mitochondrial fragmentation or fission signals the process of mitophagy [19,30,31,32].”
BackgroundSelective degradation of mitochondria by mitophagy
Kim, I., Rodriguez-Enriquez, S., & Lemasters, J. J. (2007) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2007.03.034 · Cited by 1,558
OPA1 requires mitofusin 1 to promote mitochondrial fusion
Cipolat, S., de Brito, O. M., Dal Zilio, B., & Scorrano, L. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0407043101 · Cited by 1,300
Regulation of autophagy by ROS: physiology and pathology
Scherz-Shouval, R., & Elazar, Z. (2011) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2010.07.007 · Cited by 1,263
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
Mitochondrial reactive oxygen species regulate cellular signaling and dictate biological outcomes
Hamanaka, R. B., & Chandel, N. S. (2010) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2010.04.002 · Cited by 1,011
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
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 · cited 1×
“Mdivi is the known potent Drp-1 inhibitor and has been reported of its protective role in mice models of experimental ischemia reperfusion studies in both heart and kidneys [26,33,34].”
Background
Cited by
Autophagy and mitophagy in cardiovascular disease
Bravo-San Pedro, J. M., Kroemer, G., & Galluzzi, L. (2017) · Circulation Research · doi:10.1161/circresaha.117.311082 · Cited by 843
Mitochondrial fusion and fission: The fine‐tune balance for cellular homeostasis
Adebayo, M., Singh, S., Singh, A. P., & Dasgupta, S. (2021) · The FASEB Journal · doi:10.1096/fj.202100067r · Cited by 733
Mitophagy-dependent necroptosis contributes to the pathogenesis of COPD
Mizumura, K., Cloonan, S. M., Nakahira, K., Bhashyam, A. R., Cervo, M., Kitada, T., Glass, K., Owen, C. A., Mahmood, A., Washko, G. R., et al. (2014) · Journal of Clinical Investigation · doi:10.1172/jci74985 · Cited by 611
Mitochondrial dynamics, mitophagy and cardiovascular disease
Vásquez‐Trincado, C., García‐Carvajal, I., Pennanen, C., Parra, V., Hill, J. A., Rothermel, B. A., & Lavandero, S. (2016) · The Journal of Physiology · doi:10.1113/jp271301 · Cited by 629
The pharmacological regulation of cellular mitophagy
Georgakopoulos, N. D., Wells, G., & Campanella, M. (2017) · Nature Chemical Biology · doi:10.1038/nchembio.2287 · Cited by 319
Metadata
- Authors
- Givvimani, S., Munjal, C., Tyagi, N., Sen, U., Metreveli, N., & Tyagi, S. C.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-03-27
- Volume
- 7
- Issue
- 3
- Pages
- e32388
- ISSN
- 1932-6203 (ISSN-L)
- OpenAlex
- W1991774783
- Cited by
- 203
- References
- 9
- FWCI
- 10.77
- Type
- journal article
- Language
- en
- Open access
- gold
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- Givvimani, S., Munjal, C., Tyagi, N., Sen, U., Metreveli, N., & Tyagi, S. C. (2012). Mitochondrial division/mitophagy inhibitor (Mdivi) Ameliorates Pressure Overload Induced Heart Failure. PLoS ONE. https://doi.org/10.1371/journal.pone.0032388
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