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Cyclosporine-A as a neuroprotective agent against stroke: its translation from laboratory research to clinical
Mohamed M Osman1, Dzenan Lulic, Loren Glover
1Center of Excellence in Aging and Brain Repair, Department of Neurosurgery and Brain Repair, University of South Florida College of Medicine, 12901 Bruce B. Downs Boulevard, Tampa, FL 33612, USA.
Abstract:
Stoke remains a leading cause of death and disability with limited treatment options. Extensive research has been aimed at studying cell death events that accompany stroke and how to use these same cell death pathways as potential therapeutic targets for treating the disease. The mitochondrial permeability transition pore (MPTP) has been implicated as a major factor associated with stroke-induced neuronal cell death. MPTP activation and increased permeability has been shown to contribute to the events that lead to cell death. Cyclosporine A (CsA), a widely used immunosuppressant in transplantation and rheumatic medicine, has been recently shown to possess neuroprotective properties through its ability to block the MPTP, which in turn inhibits neuronal damage. This newfound CsA-mediated neuroprotection pathway prompted research on its use to prevent cell death in stroke and other neurological conditions. Preclinical studies are being conducted in hopes of establishing the safety and efficacy guidelines for CsA use in human trials as a potential neuroprotective agent against stroke. In this review, we provide an overview of the current laboratory and clinical status of CsA neuroprotection.
Insights
Cyclosporine A (CsA) may protect brain cells from stroke-induced death by blocking the mitochondrial permeability transition pore (MPTP). Research is exploring CsA as a potential neuroprotective therapy for stroke patients.
Area of Science:
- Neuroscience
- Pharmacology
- Cell Biology
Background:
- Stroke is a major cause of death and disability with limited therapeutic options.
- Neuronal cell death pathways, particularly involving the mitochondrial permeability transition pore (MPTP), are critical in stroke pathology.
- The MPTP is implicated in stroke-induced neuronal death, making it a potential therapeutic target.
Purpose of the Study:
- To review the neuroprotective potential of Cyclosporine A (CsA) against stroke.
- To examine the mechanism by which CsA inhibits MPTP activation and subsequent neuronal damage.
- To provide an overview of the current preclinical and clinical research status of CsA for stroke treatment.
Main Methods:
- Review of existing laboratory and clinical studies on CsA and neuroprotection.
- Analysis of the role of MPTP in stroke-induced cell death.
- Investigation of CsA's mechanism of action in blocking MPTP.
Main Results:
- Cyclosporine A (CsA) demonstrates neuroprotective properties by inhibiting the mitochondrial permeability transition pore (MPTP).
- Blocking the MPTP with CsA prevents neuronal damage associated with stroke.
- Preclinical studies are evaluating the safety and efficacy of CsA for potential human trials.
Conclusions:
- CsA shows promise as a neuroprotective agent for stroke by targeting the MPTP pathway.
- Further research and clinical trials are necessary to establish CsA as a viable treatment for stroke.
- Targeting the MPTP represents a potential therapeutic strategy for mitigating stroke-related brain injury.