The DOI matches its Crossref record; 131 of the 131 references it cites were found in a registry or an index.
Mitochondrial contact sites: Their role in energy metabolism and apoptosis
Open accessAbstract
The energy metabolism of the failing heart is characterised by a 30% decrease of the total adenine nucleotides content and what may be more important by a 60% loss of creatine and creatine phosphate [J.S. Ingwall, R.G. Weiss, Is the failing heart energy starved? On using chemical energy to support cardiac function, Circ. Res. 95 (2004) 35-145]. Besides the effect of these changes on the energy supply, failing heart is known to be more vulnerable to Ca2+ overload and apoptosis-inducing processes. Recent studies have pointed to the critical role of mitochondrial contact sites in controlling both the mitochondrial energy metabolism and Ca2+ homeostasis. This review focuses on the structure and function of protein complexes in mitochondrial contact sites and their regulatory role in the cellular bioenergetics, intra- and extra-mitochondrial Ca2+ levels, and release of apoptosis-inducing factors. Firstly, we review the compositions of different contact sites following by the discussion of experimental data obtained with isolated and reconstituted voltage-dependent anion channel-adenine nucleotide translocase complexes and consequences of the complex disassembling. Furthermore, we describe experiments involving the complex-stabilizing conditions in vitro and in intact cells. At the end, we discuss unsolved problems and opportunities for clinical application of the complex-stabilizing factors.
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“Voltage-dependent anion channel is found at contact sites between the OMM and the IMM (101) where it may complex with energetics-related proteins, such as hexokinase, ANT, and creatine kinase, or with apoptotic proteins of the Bcl-2 family (18), and as noted above, and discussed below in greater detail, appears to play a central role in facilitating mitochondrial steroidogenic cholesterol”
From Adrenal Mitochondria and Steroidogenesis: From Individual Proteins to Functional Protein Assemblies (2016) · cites this paper as [18]
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Citations
Cites
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Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked
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The mitochondrial permeability transition
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Self-citationBcl-xL Regulates the Membrane Potential and Volume Homeostasis of Mitochondria
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The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore
Kokoszka, J. E., Waymire, K. G., Levy, S. E., Sligh, J. E., Cai, J., Jones, D. P., MacGregor, G. R., & Wallace, D. C. (2004) · Nature · doi:10.1038/nature02229 · Cited by 1,086
Research works printed but not linked: 1
- Basso, 2004, Cyclophilin D, cyclosporin A and the modulation of the mitochondrial permeability transition in cyclophilin D-null mice, Biophys. J., 86, 357
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Sorted by citations
Mitochondrial Reactive Oxygen Species (ROS) and ROS-Induced ROS Release
Zorov, D. B., Juhaszova, M., & Sollott, S. J. (2014) · Physiological Reviews · doi:10.1152/physrev.00026.2013 · Cited by 5,383
“There are many reviews on the tentative nature and identity of the mPTP (64, 489, 494) with details which are far beyond the scope of the present review.”
BackgroundSelf-citationPernas, L. F., & Scorrano, L. (2015) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021115-105011 · Cited by 845
The creatine kinase system and pleiotropic effects of creatine
Wallimann, T., Tokarska-Schlattner, M., & Schlattner, U. (2011) · Amino Acids · doi:10.1007/s00726-011-0877-3 · Cited by 797
“Thus, Cr is not only involved in stimulating mitochondrial respiration but also works as an effective mitochondrial protectant and anti-apoptotic compound (Brdiczka et al. 2006).”
BackgroundSteroid hormone synthesis in mitochondria
Miller, W. L. (2013) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2013.04.014 · Cited by 510
“VDAC is found at contact sites between the OMM and 422 the IMM (Mannella et al., 1992) where it may complex with hexo423 kinase, ANT, creatine kinase and proteins of the Bcl-2 family 424 (Brdiczka et al., 2006).”
The mitochondrial contact site complex, a determinant of mitochondrial architecture
Harner, M. E., Körner, C., Walther, D. M., Mokranjac, D., Kaesmacher, J., WELSCH, U. N., Griffith, J. M., Mann, M., Reggiori, F., & Neupert, W. (2011) · The EMBO Journal · doi:10.1038/emboj.2011.379 · Cited by 497
“Likewise, export of ATP from the mitochondria by a joint action of the ADP/ATP translocase, VDAC/porin and hexokinase (Brdiczka et al, 2006) may not need the presence of CS.”
Background
Metadata
- Authors
- Brdiczka, D. G., Zorov, D. B., & Sheu, S.-S.
- Affiliations
- University of Rochester Medicine (US)
- Lomonosov Moscow State University (RU)
- Corresponding author
- Brdiczka, Dieter G.
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2006-02
- Volume
- 1762
- Issue
- 2
- Pages
- 148-163
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W2114758506
- Cited by
- 150
- References
- 129
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 5 · 2023: 2 · 2022: 3 · 2021: 4 · 2020: 5 · 2019: 2 · 2018: 5 · 2017: 15 · 2016: 10 · 2015: 8 · 2014: 7 · 2013: 9 · 2012: 9
- FWCI
- 0.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2759 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association (HL-33333, 0050839T)
- New York State Department of Health
- National Institutes of Health (0050839T)
- National Heart, Lung, and Blood Institute (HL 33333, R01HL033333)
- National Institute of Neurological Disorders and Stroke (NS-37710, R01NS037710)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › ATP Synthase and ATPases Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- mitochondrial contact sites, mitochondrial bioenergetics, apoptosis, heart failure, voltage-dependent anion channel, adenine nucleotide translocase, mitochondrial calcium homeostasis, mitochondrial protein complexes, complex stabilization, calcium overload
- MeSH terms
- Mitochondrial ADP, ATP Translocases, Animals, Energy Metabolism, Mitochondria, Apoptosis, Cytochromes c, Mitochondrial Membranes
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