The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Depressed mitochondrial transcription factors and oxidative capacity in rat failing cardiac and skeletal muscles
Open accessAbstract
Congestive heart failure (CHF) induces alterations in energy metabolism and mitochondrial function that span cardiac as well as skeletal muscles. Whether these defects originate from altered mitochondrial DNA copy number and/or mitochondrial gene transcription is not known at present, nor are the factors that control mitochondrial capacity in different muscle types completely understood. We used an experimental model of CHF induced by aortic banding in the rat and investigated mitochondrial respiration and enzyme activity of biochemical mitochondrial markers in cardiac, slow and fast skeletal muscles. We quantified mitochondrial DNA (mtDNA), expression of nuclear (COX IV) and mitochondrial (COX I) encoded cytochrome c oxidase subunits as well as nuclear factors involved in mitochondrial biogenesis and in the necessary coordinated interplay between nuclear and mitochondrial genomes in health and CHF. CHF induced a decrease in oxidative capacity and mitochondrial enzyme activities with a parallel decrease in the mRNA level of COX I and IV, but no change in mtDNA content. The expression of the peroxisome proliferator activated receptor gamma co‐activator 1α (PGC‐1α) gene was downregulated in CHF, as well as nuclear respiratory factor 2 and mitochondrial transcription factor A, which act downstream from PGC‐1α. Most interestingly, only the level of PGC‐1α expression was strongly correlated with muscle oxidative capacity in cardiac and skeletal muscles, both in healthy and CHF rats. Mitochondrial gene transcription is reduced in CHF, and PGC‐1α appears as a potential modulator of muscle oxidative capacity under these experimental conditions.
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Cites
Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres
Lin, J., Wu, H., Tarr, P. T., Zhang, C.-Y., Wu, Z., Boss, O., Michael, L. F., Puigserver, P., Isotani, E., Olson, E. N., et al. (2002) · Nature · doi:10.1038/nature00904 · Cited by 2,546
Peroxisome proliferator–activated receptor γ coactivator-1 promotes cardiac mitochondrial biogenesis
Lehman, J. J., Barger, P. M., Kovacs, A., Saffitz, J. E., Medeiros, D. M., & Kelly, D. P. (2000) · Journal of Clinical Investigation · doi:10.1172/jci10268 · Cited by 1,285
Mitochondrial transcription factors B1 and B2 activate transcription of human mtDNA
Falkenberg, M., Gaspari, M., Rantanen, A., Trifunovic, A., Larsson, N.-G., & Gustafsson, C. M. (2002) · Nature Genetics · doi:10.1038/ng909 · Cited by 598 · cited 2×
“It was recently established that replication of mtDNA was stimulated by small amounts of mtTFA and remained highly active over a large range of mtTFA concentrations whereas transcription was activated only at high levels of mtTFA (Falkenberg et al. 2002).”
BackgroundWang, J., Wilhelmsson, H., Graff, C., Li, H., Oldfors, A., Rustin, P., Brüning, J. C., Kahn, C. R., Clayton, D. A., Barsh, G. S., et al. (1999) · Nature Genetics · doi:10.1038/5089 · Cited by 435
Czubryt, M. P., McAnally, J., Fishman, G. I., & Olson, E. N. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0337639100 · Cited by 418
Transcriptional Activation Of Energy Metabolic Switches In The Developing And Hypertrophied Heart
Lehman, J. J., & Kelly, D. P. (2002) · Clinical and Experimental Pharmacology and Physiology · doi:10.1046/j.1440-1681.2002.03655.x · Cited by 257
Transcriptional effects of chronic Akt activation in the heart
Cook, S. A., Matsui, T., Li, L., & Rosenzweig, A. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m201462200 · Cited by 199
Genetic modification of survival in tissue-specific knockout mice with mitochondrial cardiomyopathy
Li, H., Wang, J., Wilhelmsson, H., Hansson, A., Thorén, P., Duffy, J., Rustin, P., & Larsson, N.-G. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.97.7.3467 · Cited by 185
Cited by
Role of Mitochondrial Dysfunction in Insulin Resistance
Kim, J.-A., Wei, Y., & Sowers, J. R. (2008) · Circulation Research · doi:10.1161/circresaha.107.165472 · Cited by 1,103
Transcriptional control of mitochondrial biogenesis: the central role of PGC-1
Ventura-Clapier, R., Garnier, A., & Veksler, V. (2008) · Cardiovascular Research · doi:10.1093/cvr/cvn098 · Cited by 932
Self-citationArany, Z., He, H., Lin, J., Hoyer, K., Handschin, C., Toka, O., Ahmad, F., Matsui, T., Chin, S., Wu, P.-H., et al. (2005) · Cell Metabolism · doi:10.1016/j.cmet.2005.03.002 · Cited by 694
Is the Failing Heart Energy Starved?: On Using Chemical Energy to Support Cardiac Function
Ingwall, J. S., & Weiss, R. G. (2004) · Circulation Research · doi:10.1161/01.res.0000137170.41939.d9 · Cited by 604
Energy metabolism in heart failure
Ventura‐Clapier, R., Garnier, A., & Veksler, V. (2004) · The Journal of Physiology · doi:10.1113/jphysiol.2003.055095 · Cited by 499
Self-citation
Metadata
- Authors
- Garnier, A., Fortin, D., Deloménie, C., Momken, I., Veksler, V., & Ventura‐Clapier, R.
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2003-09
- Volume
- 551
- Issue
- 2
- Pages
- 491-501
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- OpenAlex
- W2165547205
- Cited by
- 427
- References
- 8
- FWCI
- 4.93
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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