Mitochondria and Cardiac Hypertrophy.
Abstract
Cardiac tissue responds to long-term hemodynamic load through initiation of a hypertrophic remodeling program. Importantly, if not counteracted this response will eventually lead to organ failure. Cardiac hypertrophic adaptations are complex, and involve multiple cellular events and the mechanisms underlying the development of cardiac hypertrophy are not well understood. Mitochondrial dysfunction has been indicated as a potential and important player in the development of cardiac hypertrophy. Additionally, substantial evidence shows that a significant portion of mitochondrial processes, necessary for normal cardiomyocyte physiology, are impacted by these hypertrophic changes. In this chapter, we will present and discuss the adaptations and changes in the mitochondrial electron transport system, mitochondrial metabolism, mitochondrial biogenesis, oxidative stress, the opening of the mitochondrial permeability transition pore following hypertrophic stimuli, as well as, review the various drugs (targeting mitochondria) that can be used in treatment of cardiac hypertrophy.
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The half-life of mitochondria is a couple of weeks in several cell types.
“The half-life of mitochondria is known to be a couple of weeks in several cell types,20”
From ApoE4-dependent lysosomal cholesterol accumulation impairs mitochondrial homeostasis and oxidative phosphorylation in human astrocytes (2023) · cites this paper as [21]
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References 168 · Cited by 70
- Authors
- Facundo, H. D. T. F., Brainard, R. E., Caldas, F. R. D. L., & Lucas, A. M. B.
- Affiliations
- Valencia College (US)
- Instituto Federal de Educação, Ciência e Tecnologia do Ceará (BR)
- Universidade Federal do Cariri (BR)
- Venue
- Advances in Experimental Medicine and Biology
- Publisher
- Springer International Publishing
- Published
- 2017
- Volume
- 982
- Pages
- 203-226
- ISSN
- 0065-2598 (ISSN-L)
- 2214-8019
- OpenAlex
- W2618072884
- Cited by
- 70
- References
- 168
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 10 · 2023: 6 · 2022: 12 · 2021: 9 · 2020: 12 · 2019: 3 · 2018: 7 · 2017: 1
- FWCI
- 7.79
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Advances in experimental medicine and biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- cardiac hypertrophy, mitochondrial dysfunction, mitochondrial electron transport chain, mitochondrial metabolism, mitochondrial biogenesis, oxidative stress, mitochondrial permeability transition pore, hemodynamic load, cardiac remodeling, mitochondrial-targeted drugs
- MeSH terms
- Mitochondrial Permeability Transition Pore, Animals, Organelle Biogenesis, Calcium, Energy Metabolism, Cardiomegaly, Humans, Mitochondria, Heart, Oxidative Stress, Calcium Signaling, Myocytes, Cardiac, Mitochondrial Membrane Transport Proteins, Mitochondrial Dynamics
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