The DOI matches its Crossref record; 54 of the 55 references it cites were found in a registry or an index.
Exercise reestablishes autophagic flux and mitochondrial quality control in heart failure
Open accessAbstract
-induced mitochondrial permeability transition pore opening. Of interest, disruption of autophagic flux was sufficient to decrease cardiac mitochondrial function in sham-treated animals and increase cardiomyocyte toxicity upon mitochondrial stress. Importantly, 8 wk of exercise training, starting 4 wk after myocardial infarction at a time when autophagy and mitochondrial oxidative capacity were already impaired, improved cardiac autophagic flux. These changes were followed by reduced mitochondrial number:size ratio, increased mitochondrial bioenergetics and better cardiac function. Moreover, exercise training increased cardiac mitochondrial number, size and oxidative capacity without affecting autophagic flux in sham-treated animals. Further supporting an autophagy mechanism for exercise-induced improvements of mitochondrial bioenergetics in heart failure, acute in vivo inhibition of autophagic flux was sufficient to mitigate the increased mitochondrial oxidative capacity triggered by exercise in failing hearts. Collectively, our findings uncover the potential contribution of exercise in restoring cardiac autophagy flux in heart failure, which is associated with better mitochondrial quality control, bioenergetics and cardiac function.
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“Moreover, exercise is the best non-pharmacological strategy to reactivate mitophagy, which reduces the accumulation of ROS and thus, improves mitochondrial health and delays the loss of muscle mass that accompanies various pathologies, including aging sarcopenia, heart failure and neurogenic myopathy [224, 238–240].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [239]
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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
Heart Disease and Stroke Statistics—2015 Update: A Report From the American Heart Association
Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman, M., de Ferranti, S., Després, J.-P., Fullerton, H. J., Howard, V. J., et al. (2015) · Circulation · doi:10.1161/cir.0000000000000152 · Cited by 5,797
Hunt, S. A., Abraham, W. T., Chin, M. H., Feldman, A. M., Francis, G. S., Ganiats, T. G., Jessup, M. L., Konstam, M. A., MANCINI, D. M., Michl, K., et al. (2009) · Circulation · doi:10.1161/circulationaha.109.192065 · Cited by 3,739
During autophagy mitochondria elongate, are spared from degradation and sustain cell viability
Gomes, L. C., Benedetto, G. D., & Scorrano, L. (2011) · Nature Cell Biology · doi:10.1038/ncb2220 · Cited by 1,735
The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress
Nakai, A., Yamaguchi, O., Takeda, T., Higuchi, Y., Hikoso, S., Taniike, M., Omiya, S., Mizote, I., Matsumura, Y., Asahi, M., et al. (2007) · Nature Medicine · doi:10.1038/nm1574 · Cited by 1,520
Proteasome and p97 mediate mitophagy and degradation of mitofusins induced by Parkin
Tanaka, A., Cleland, M. M., Xu, S., Narendra, D. P., Suen, D.-F., Karbowski, M., & Youle, R. J. (2010) · Journal of Cell Biology · doi:10.1083/jcb.201007013 · Cited by 1,369
Mitochondrial Dynamics in the Regulation of Nutrient Utilization and Energy Expenditure
Liesa, M., & Shirihai, O. S. (2013) · Cell Metabolism · doi:10.1016/j.cmet.2013.03.002 · Cited by 1,341
PINK1-Phosphorylated Mitofusin 2 Is a Parkin Receptor for Culling Damaged Mitochondria
Chen, Y., & Dorn, G. W. (2013) · Science · doi:10.1126/science.1231031 · Cited by 1,323
Mitochondrial DNA that escapes from autophagy causes inflammation and heart failure
Oka, T., Hikoso, S., Yamaguchi, O., Taneike, M., Takeda, T., Tamai, T., Oyabu, J., Murakawa, T., Nakayama, H., Nishida, K., et al. (2012) · Nature · doi:10.1038/nature10992 · Cited by 1,201
Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis
He, C., Bassik, M. C., Moresi, V., Sun, K., Wei, Y., Zou, Z., An, Z., Loh, J., Fisher, J., Sun, Q., et al. (2012) · Nature · doi:10.1038/nature10758 · Cited by 1,136
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Metadata
- Authors
- Campos, J. C., Queliconi, B. B., Bozi, L. H. M., Bechara, L. R. G., Dourado, P. M. M., Andres, A. M., Jannig, P. R., Gomes, K. M. S., Zambelli, V. O., Rocha-Resende, C., Guatimosim, S., Brum, P. C., Mochly-Rosen, D., Gottlieb, R. A., Kowaltowski, A. J., & Ferreira, J. C. B.
- Affiliations
- Cedars-Sinai Medical Center (US)
- Universidade de São Paulo (BR)
- Department of Anatomy, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil
- Instituto Butantan (BR)
- Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Brazil
- School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, Brazil
- Department of Chemical and Systems Biology, Stanford University School of Medicine, Stanford, CA, USA
- Corresponding author
- Ferreira, Julio C. B.
- ORCID
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2017-08-03
- Volume
- 13
- Issue
- 8
- Pages
- 1304-1317
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- PMC
- PMC5584854
- OpenAlex
- W2624424641
- Cited by
- 146
- References
- 55
- Citations by year
- 2026: 9 · 2025: 15 · 2024: 12 · 2023: 15 · 2022: 25 · 2021: 21 · 2020: 21 · 2019: 15 · 2018: 10 · 2017: 3
- FWCI
- 10.46
- Type
- journal article
- Language
- en
- Update notices
- correction (2024-03-21)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Autophagy (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institute on Alcohol Abuse and Alcoholism (R37AA011147)
- National Heart, Lung, and Blood Institute (R01HL052141, P01HL112730, R01HL132075)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Keywords
- exercise training, autophagic flux, mitochondrial quality control, heart failure, myocardial infarction, mitochondrial permeability transition pore, mitochondrial bioenergetics, cardiomyocyte toxicity, mitochondrial oxidative capacity, cardiac function
- MeSH terms
- Animals, Autophagy, Cell Line, Cell Survival, Heart Failure, Male, Mitochondria, Physical Conditioning, Animal, Down-Regulation, Rats, Wistar, Mice, Mitochondrial Dynamics
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