ArticleThe Biochemical journal2009
Mitochondrial targeting of cyclosporin A enables selective inhibition of cyclophilin-D and enhanced cytoprotection after glucose and oxygen deprivation.
Article in The Biochemical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 68 citations in OpenAlex.
- Mitochondria-Targeting Moieties Based on N-Tethered Pyridinium Cations.Angewandte Chemie (International ed. in English) · 2026Article
- Molecular and Cellular Mechanisms of Myocardial Ischemia and Reperfusion Injury: A Narrative Review.Cells · 2026Review
- Lipophilic Cations as Mitochondria-Targeting Moieties: Recent Progress and Design Principles for Medicinal Chemistry.Journal of medicinal chemistry · 2025Review
- Non-Immunosuppressive Cyclophilin Inhibitors.Angewandte Chemie (International ed. in English) · 2022Review
- Immunosuppression-related neurological disorders in kidney transplantation.Journal of nephrology · 2021Review
- Cyclophilin D, Somehow a Master Regulator of Mitochondrial Function.Biomolecules · 2018Review
- Mitochondrial permeability transition pore: a potential drug target for neurodegeneration.Drug discovery today · 2018Review
- Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases.International review of cell and molecular biology · 2018Review
- Infection Counter: Automated Quantification of in Vitro Virus Replication by Fluorescence Microscopy.Viruses · 2016Article
- Selective Inhibition of the Mitochondrial Permeability Transition Pore Protects against Neurodegeneration in Experimental Multiple Sclerosis.The Journal of biological chemistry · 2016Article
- Cyclosporin A promotes tumor angiogenesis in a calcineurin-independent manner by increasing mitochondrial reactive oxygen species.Molecular cancer research : MCR · 2014Article
- Inhibition of cyclophilin D by cyclosporin A promotes retinal ganglion cell survival by preventing mitochondrial alteration in ischemic injury.Cell death & disease · 2014Article
- Cyclosporine A-nanoparticles enhance the therapeutic benefit of adipose tissue-derived stem cell transplantation in a swine myocardial infarction model.International journal of nanomedicine · 2014Article
- Cyclophilin D extramitochondrial signaling controls cell cycle progression and chemokine-directed cell motility.The Journal of biological chemistry · 2013Article
- Resveratrol-sensitized UVA induced apoptosis in human keratinocytes through mitochondrial oxidative stress and pore opening.Journal of photochemistry and photobiology. B, Biology · 2012Article
- Cyclosporin A and cardioprotection: from investigative tool to therapeutic agent.British journal of pharmacology · 2012Review
- A mitochondrial-targeted cyclosporin A with high binding affinity for cyclophilin D yields improved cytoprotection of cardiomyocytes.The Biochemical journal · 2012Article
- Selective uncoupling of individual mitochondria within a cell using a mitochondria-targeted photoactivated protonophore.Journal of the American Chemical Society · 2012Article
- Inhibition of the Mitochondrial Permeability Transition for Cytoprotection: Direct versus Indirect Mechanisms.Biochemistry research international · 2012Article
- An approach to experimental synaptic pathology using green fluorescent protein-transgenic mice and gene knockout mice to show mitochondrial permeability transition pore-driven excitotoxicity in interneurons and motoneurons.Toxicologic pathology · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
CsA (cyclosporin A) is a hydrophobic undecapeptide that inhibits CyPs (cyclophilins), a family of PPIases (peptidylprolyl cis-trans isomerases). In some experimental models, CsA offers partial protection against lethal cell injury brought about by transient ischaemia; this is believed to reflect inhibition of CyP-D, a mitochondrial isoform that facilitates formation of the permeability transition pore in the mitochondrial inner membrane. To evaluate this further, we have targeted CsA to mitochondria so that it becomes selective for CyP-D in cells. This was achieved by conjugating the inhibitor to the lipophilic triphenylphosphonium cation, enabling its accumulation in mitochondria due to the inner membrane potential. In a cell-free system and in B50 neuroblastoma cells the novel reagent (but not CsA itself) preferentially inhibited CyP-D over extramitochondrial CyP-A. In hippocampal neurons, mitochondrial targeting markedly enhanced the capacity of CsA to prevent cell necrosis brought about by oxygen and glucose deprivation, but largely abolished its capacity to inhibit glutamate-induced cell death. It is concluded that CyP-D has a major pathogenic role in 'energy failure', but not in glutamate excitotoxicity, where cytoprotection primarily reflects CsA interaction with extramitochondrial CyPs and calcineurin. Moreover, the therapeutic potential of CsA against ischaemia/reperfusion injuries not involving glutamate may be improved by mitochondrial targeting.
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