The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.
Mitochondrial Complex I Deficiency Increases Protein Acetylation and Accelerates Heart Failure
Open accessAbstract
Summary Mitochondrial respiratory dysfunction is linked to the pathogenesis of multiple diseases including heart failure but the specific mechanisms for this link remain largely elusive. We modeled the impairment of mitochondrial respiration by inactivation of the Ndufs4 gene, a protein critical for Complex I (C-I) assembly, in the mouse heart (cKO). While C-I supported respiration decreased by >40%, the cKO mice maintained normal cardiac function in vivo and high-energy phosphate content in isolated perfused hearts. However, the cKO mice developed accelerated heart failure after pressure overload or repeated pregnancy. Decreased NAD+/NADH ratio by C-I deficiency inhibited Sirt3 activity, leading to increase in protein acetylation, and sensitization of the permeability transition in mitochondria (mPTP). NAD+ precursor supplementation to cKO mice partially normalized the NAD+/NADH ratio, protein acetylation and mPTP sensitivity. These findings describe a mechanism connecting mitochondrial dysfunction to the susceptibility to diseases and propose a potential therapeutic target.
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Cites
2 retracted
Sirtuin-3 deacetylation of cyclophilin D induces dissociation of hexokinase II from the mitochondria
Shulga, N., Wilson-Smith, R., & Pastorino, J. G. (2010) · Journal of Cell Science · doi:10.1242/jcs.061846 · Cited by 163
RetractedShulga, N., & Pastorino, J. G. (2010) · Journal of Cell Science · doi:10.1242/jcs.073502 · Cited by 77
RetractedThe Failing Heart — An Engine Out of Fuel
Neubauer, S. (2007) · New England Journal of Medicine · doi:10.1056/nejmra063052 · Cited by 2,417
Wittig, I., Braun, H.-P., & Schägger, H. (2006) · Nature Protocols · doi:10.1038/nprot.2006.62 · Cited by 1,708
Mitochondrial Respiratory-Chain Diseases
DiMauro, S., & Schon, E. A. (2003) · New England Journal of Medicine · doi:10.1056/nejmra022567 · Cited by 1,661
Sirt5 Is a NAD-Dependent Protein Lysine Demalonylase and Desuccinylase
Du, J., Zhou, Y., Su, X., Yu, J. J., Khan, S., Jiang, H., Kim, J., Woo, J., Kim, J. H., Choi, B. H., et al. (2011) · Science · doi:10.1126/science.1207861 · Cited by 1,429
Reactive Oxygen Species (Ros-Induced) Ros Release
Zorov, D. B., Filburn, C. R., Klotz, L.-O., Zweier, J. L., & Sollott, S. J. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.192.7.1001 · Cited by 1,412
Yoshino, J., Mills, K. F., Yoon, M. J., & Imai, S.-I. (2011) · Cell Metabolism · doi:10.1016/j.cmet.2011.08.014 · Cited by 1,340
Generation of reactive oxygen species by the mitochondrial electron transport chain
Liu, Y., Fiskum, G., & Schubert, D. (2002) · Journal of Neurochemistry · doi:10.1046/j.0022-3042.2002.00744.x · Cited by 1,260
Mammalian Sir2 homolog SIRT3 regulates global mitochondrial lysine acetylation
Lombard, D. B., Alt, F. W., Cheng, H.-L., Bunkenborg, J., Streeper, R. S., Mostoslavsky, R., Kim, J., Yancopoulos, G., Valenzuela, D., Murphy, A., et al. (2007) · Molecular and Cellular Biology · doi:10.1128/mcb.01636-07 · Cited by 1,216
Cited by
NAD+ and sirtuins in aging and disease
Imai, S.-I., & Guarente, L. (2014) · Trends in Cell Biology · doi:10.1016/j.tcb.2014.04.002 · Cited by 1,481
Cardiac Energy Metabolism in Heart Failure
Lopaschuk, G. D., Karwi, Q. G., Tian, R., Wende, A. R., & Abel, E. D. (2021) · Circulation Research · doi:10.1161/circresaha.121.318241 · Cited by 1,373
Self-citationNAD + in aging, metabolism, and neurodegeneration
Verdin, E. (2015) · Science · doi:10.1126/science.aac4854 · Cited by 1,319
NAD+ Intermediates: The Biology and Therapeutic Potential of NMN and NR
Yoshino, J., Baur, J. A., & Imai, S.-I. (2018) · Cell Metabolism · doi:10.1016/j.cmet.2017.11.002 · Cited by 1,061
NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential
Xie, N., Zhang, L., Gao, W., Huang, C., Huber, P. E., Zhou, X., Li, C., Shen, G., & Zou, B. (2020) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-020-00311-7 · Cited by 1,052
Metadata
- Authors
- Karamanlidis, G., Lee, C. F., Garcia-Menendez, L., Kolwicz, S. C., Suthammarak, W., Gong, G., Sedensky, M. M., Morgan, P. G., Wang, W., & Tian, R.
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2013-08
- Volume
- 18
- Issue
- 2
- Pages
- 239-250
- ISSN
- 1550-4131 (ISSN-L)
- OpenAlex
- W2023657018
- Cited by
- 468
- References
- 46
- FWCI
- 13.18
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Karamanlidis, G., Lee, C. F., Garcia-Menendez, L., Kolwicz, S. C., Suthammarak, W., Gong, G., Sedensky, M. M., Morgan, P. G., Wang, W., & Tian, R. (2013). Mitochondrial Complex I Deficiency Increases Protein Acetylation and Accelerates Heart Failure. Cell Metabolism. https://doi.org/10.1016/j.cmet.2013.07.002
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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