The DOI matches its Crossref record; 244 of the 244 references it cites were found in a registry or an index.
Mitochondrial function as a therapeutic target in heart failure
Open accessAbstract
The pathophysiology of heart failure is complex, but mitochondrial dysfunction is an emerging therapeutic target to improve cardiac function. In this Consensus Statement, insights into the mechanisms of mitochondrial dysfunction in heart failure are presented, along with an overview of emerging treatments with the potential to improve the function of the failing heart by targeting mitochondria. Heart failure is a pressing worldwide public-health problem with millions of patients having worsening heart failure. Despite all the available therapies, the condition carries a very poor prognosis. Existing therapies provide symptomatic and clinical benefit, but do not fully address molecular abnormalities that occur in cardiomyocytes. This shortcoming is particularly important given that most patients with heart failure have viable dysfunctional myocardium, in which an improvement or normalization of function might be possible. Although the pathophysiology of heart failure is complex, mitochondrial dysfunction seems to be an important target for therapy to improve cardiac function directly. Mitochondrial abnormalities include impaired mitochondrial electron transport chain activity, increased formation of reactive oxygen species, shifted metabolic substrate utilization, aberrant mitochondrial dynamics, and altered ion homeostasis. In this Consensus Statement, insights into the mechanisms of mitochondrial dysfunction in heart failure are presented, along with an overview of emerging treatments with the potential to improve the function of the failing heart by targeting mitochondria.
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2013 ACCF/AHA Guideline for the Management of Heart Failure
Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Drazner, M. H., Fonarow, G. C., Geraci, S. A., Horwich, T., Januzzi, J. L., et al. (2013) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2013.05.019 · Cited by 12,536
Self-citationHow mitochondria produce reactive oxygen species
Murphy, M. P. (2009) · Biochemical Journal · doi:10.1042/bj20081386 · Cited by 8,207
Control of inositol 1,4,5-trisphosphate-induced Ca2+ release by cytosolic Ca2+
Bootman, M. D., Missiaen, L., Parys, J. B., De Smedt, H., & Casteels, R. (1995) · Biochemical Journal · doi:10.1042/bj3060445 · Cited by 5,120
Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism
MITCHELL, P. (1961) · Nature · doi:10.1038/191144a0 · Cited by 4,704
ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult
Hunt, S. A. (2005) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2005.08.022 · Cited by 4,154
2005 WRITING COMMITTEE MEMBERS, Hunt, S. A., Abraham, W. T., Chin, M. H., Feldman, A. M., Francis, G. S., Ganiats, T. G., Jessup, M., Konstam, M. A., Mancini, D. M., et al. (2009) · Circulation · doi:10.1161/circulationaha.109.192065 · Cited by 3,720
Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS
Chouchani, E. T., Pell, V. R., Gaude, E., Aksentijević, D., Sundier, S. Y., Robb, E. L., Logan, A., Nadtochiy, S. M., Ord, E. N. J., Smith, A. C., et al. (2014) · Nature · doi:10.1038/nature13909 · Cited by 2,907
Baines, C. P., Kaiser, R. A., Purcell, N. H., Blair, N. S., Osinska, H., Hambleton, M. A., Brunskill, E. W., Sayen, M. R., Gottlieb, R. A., Dorn, G. W., et al. (2005) · Nature · doi:10.1038/nature03434 · Cited by 2,280
WRITING COMMITTEE MEMBERS, Hunt, S. A., Abraham, W. T., Chin, M. H., Feldman, A. M., Francis, G. S., Ganiats, T. G., Jessup, M., Konstam, M. A., Mancini, D. M., et al. (2005) · Circulation · doi:10.1161/circulationaha.105.167586 · Cited by 2,251
O'Connor (2009) · doi:10.1001/jama.2009.454 · Cited by 2,173
Cited by
Repairing mitochondrial dysfunction in disease
Sorrentino, V., Menzies, K. J., & Auwerx, J. (2018) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev-pharmtox-010716-104908 · Cited by 337
Wang, B., Nie, J., Wu, L., Hu, Y., Wen, Z., Dong, L., Zou, M.-H., Chen, C., & Wang, D. W. (2018) · Circulation Research · doi:10.1161/circresaha.117.312317 · Cited by 334
Mitochondrial Dysfunction in Heart Failure With Preserved Ejection Fraction
Kumar, A. A., Kelly, D. P., & Chirinos, J. A. (2019) · Circulation · doi:10.1161/circulationaha.118.036259 · Cited by 298
Zinovkin, R. A., & Zamyatnin, A. A. (2019) · Current Molecular Pharmacology · doi:10.2174/1874467212666181127151059 · Cited by 209
The Involvement of Mg2+ in Regulation of Cellular and Mitochondrial Functions
Pilchova, I., Klacanova, K., Tatarkova, Z., Kaplan, P., & Racay, P. (2017) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2017/6797460 · Cited by 198
Metadata
- Authors
- Brown, D. A., Perry, J. B., Allen, M. E., Sabbah, H. N., Stauffer, B. L., Shaikh, S. R., Cleland, J. G. F., Colucci, W. S., Butler, J., Voors, A. A., Anker, S. D., Pitt, B., Pieske, B., Filippatos, G., Greene, S. J., & Gheorghiade, M.
- Venue
- Nature Reviews Cardiology
- Published
- 2016-12-22
- Volume
- 14
- Issue
- 4
- Pages
- 238-250
- ISSN
- 1759-5002 (ISSN-L)
- 1759-5010
- OpenAlex
- W2565443325
- Cited by
- 803
- References
- 244
- FWCI
- 3.63
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Brown, D. A., Perry, J. B., Allen, M. E., Sabbah, H. N., Stauffer, B. L., Shaikh, S. R., Cleland, J. G. F., Colucci, W. S., Butler, J., Voors, A. A., Anker, S. D., Pitt, B., Pieske, B., Filippatos, G., Greene, S. J., & Gheorghiade, M. (2017). Mitochondrial function as a therapeutic target in heart failure. Nature Reviews Cardiology. https://doi.org/10.1038/nrcardio.2016.203
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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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