The DOI matches its Crossref record; 168 of the 168 references it cites were found in a registry or an index.
First‐in‐class cardiolipin‐protective compound as a therapeutic agent to restore mitochondrial bioenergetics
Open accessAbstract
A decline in energy is common in aging, and the restoration of mitochondrial bioenergetics may offer a common approach for the treatment of numerous age‐associated diseases. Cardiolipin is a unique phospholipid that is exclusively expressed on the inner mitochondrial membrane where it plays an important structural role in cristae formation and the organization of the respiratory complexes into supercomplexes for optimal oxidative phosphorylation. The interaction between cardiolipin and cytochrome c determines whether cytochrome c acts as an electron carrier or peroxidase. Cardiolipin peroxidation and depletion have been reported in a variety of pathological conditions associated with energy deficiency, and cardiolipin has been identified as a target for drug development. This review focuses on the discovery and development of the first cardiolipin‐protective compound as a therapeutic agent. SS‐31 is a member of the S zeto‐S chiller (SS) peptides known to selectively target the inner mitochondrial membrane. SS‐31 binds selectively to cardiolipin via electrostatic and hydrophobic interactions. By interacting with cardiolipin, SS‐31 prevents cardiolipin from converting cytochrome c into a peroxidase while protecting its electron carrying function. As a result, SS‐31 protects the structure of mitochondrial cristae and promotes oxidative phosphorylation. SS‐31 represents a new class of compounds that can recharge the cellular powerhouse and restore bioenergetics. Extensive animal studies have shown that targeting such a fundamental mechanism can benefit highly complex diseases that share a common pathogenesis of bioenergetics failure. This review summarizes the mechanisms of action and therapeutic potential of SS‐31 and provides an update of its clinical development programme. Linked Articles: This article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2014.171.issue‐8
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Cites
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“Previous research has shown that PGC-1α, a co-activator of the PPARγ, plays a major role in mitochondrial biogenesis and oxidative metabolism (Lin et al., 2005).”
BackgroundCytochrome C -Mediated Apoptosis
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Cited by
Mitochondrial dysfunction and oxidative stress in heart disease
Peoples, J. N., Saraf, A., Ghazal, N., Pham, T. T., & Kwong, J. Q. (2019) · Experimental & Molecular Medicine · doi:10.1038/s12276-019-0355-7 · Cited by 950
Microglial cell dysregulation in brain aging and neurodegeneration
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Mitochondrial Dysfunction and Biogenesis in Neurodegenerative diseases: Pathogenesis and Treatment
Golpich, M., Amini, E., Mohamed, Z., Azman Ali, R., Mohamed Ibrahim, N., & Ahmadiani, A. (2017) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.12655 · Cited by 532
Mitochondrial quality control in kidney injury and repair
Tang, C., Cai, J., Yin, X.-M., Weinberg, J. M., Venkatachalam, M. A., & Dong, Z. (2021) · Nature Reviews Nephrology · doi:10.1038/s41581-020-00369-0 · Cited by 513
Amyloid Beta and Phosphorylated Tau-Induced Defective Autophagy and Mitophagy in Alzheimer’s Disease
Reddy, P. H., & Oliver, D. M. (2019) · Cells · doi:10.3390/cells8050488 · Cited by 496
“Furthermore, loss of phospholipids—particularly the cardiolipin of the IMM—exacerbates the pathology of AD [71].”
Background
Metadata
- Authors
- Szeto, H. H.
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2014-03-28
- Volume
- 171
- Issue
- 8
- Pages
- 2029-2050
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- OpenAlex
- W1722845210
- Cited by
- 548
- References
- 168
- FWCI
- 8.74
- Type
- journal article
- Language
- en
- Open access
- bronze
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