ArticleJournal of geriatric cardiology : JGC2014
Phosphodiesterase-3 inhibitor (cilostazol) attenuates oxidative stress-induced mitochondrial dysfunction in the heart.
Article in Journal of geriatric cardiology : JGC, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Nano-Cilostazol Mitigates Cisplatin-Induced Nephrotoxicity in Rats via Modulation of Oxidative Stress, Apoptosis, Pyroptosis, and miRNA-155 Signaling.Antioxidants (Basel, Switzerland) · 2026Article
- Cilostazol protective effect on nedaplatin-induced genotoxicity in cultured human lymphocytes.Toxicology reports · 2025Article
- Cilostazol geno-protective effects mitigate carbamazepine-induced genotoxicity in human cultured blood lymphocytes.Toxicology reports · 2024Article
- Theoretical Investigations on Free Energy of Binding Cilostazol with Different Cyclodextrins as Complex for Selective PDE3 Inhibition.Molecules (Basel, Switzerland) · 2024Article
- Cilostazol Ameliorates Motor Dysfunction and Schwann Cell Impairment in Streptozotocin-Induced Diabetic Rats.International journal of molecular sciences · 2024Article
- Pimobendan prevents cardiac dysfunction, mitigates cardiac mitochondrial dysfunction, and preserves myocyte ultrastructure in a rat model of mitral regurgitation.BMC veterinary research · 2023Article
- Cilostazol attenuates oxidative stress and apoptosis in the quadriceps muscle of the dystrophic mouse experimental model.International journal of experimental pathology · 2023Article
- Cilostazol attenuates cardiac oxidative stress and inflammation in hypercholesterolemic rats.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Cilostazol for Secondary Stroke Prevention: History, Evidence, Limitations, and Possibilities.Stroke · 2021Review
- Could cilostazol be beneficial in COVID-19 treatment? Thinking about phosphodiesterase-3 as a therapeutic target.International immunopharmacology · 2021Review
- Cilostazol protects hepatocytes against alcohol-induced apoptosis via activation of AMPK pathway.PloS one · 2019Article
- Improved thrombolytic effect with focused ultrasound and neuroprotective agent against acute carotid artery thrombosis in rat.Scientific reports · 2017Article
- Development of Therapeutics That Induce Mitochondrial Biogenesis for the Treatment of Acute and Chronic Degenerative Diseases.Journal of medicinal chemistry · 2016Review
- In vivo study of the effects of exogenous hydrogen sulfide on lung mitochondria in acute lung injury in rats.BMC anesthesiology · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCilostazol is a type 3 phosphodiesterase inhibitor which has been previously demonstrated to prevent the occurrence of tachyarrhythmia and improve defibrillation efficacy. However, the mechanism for this beneficial effect is still unclear. Since cardiac mitochondria have been shown to play a crucial role in fatal cardiac arrhythmias and that oxidative stress is one of the main contributors to arrhythmia generation, we tested the effects of cilostazol on cardiac mitochondria under severe oxidative stress.
methodsMitochondria were isolated from rat hearts and treated with H2O2 to induce oxidative stress. Cilostazol, at various concentrations, was used to study its protective effects. Pharmacological interventions, including a mitochondrial permeability transition pore (mPTP) blocker, cyclosporine A (CsA), and an inner membrane anion channel (IMAC) blocker, 4'-chlorodiazepam (CDP), were used to investigate the mechanistic role of cilostazol on cardiac mitochondria. Cardiac mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential change and mitochondrial swelling were determined as indicators of cardiac mitochondrial function.
resultsCilostazol preserved cardiac mitochondrial function when exposed to oxidative stress by preventing mitochondrial depolarization, mitochondrial swelling, and decreasing ROS production.
conclusionsOur findings suggest that cardioprotective effects of cilostazol reported previously could be due to its prevention of cardiac mitochondrial dysfunction caused by severe oxidative stress.
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