ArticleCell biochemistry and biophysics2022
FIsetin Preserves Interfibrillar Mitochondria to Protect Against Myocardial Ischemia-Reperfusion Injury.
Article in Cell biochemistry and biophysics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Effects and Mechanisms of Fisetin against Ischemia-reperfusion Injuries: A Systematic Review.Current pharmaceutical biotechnology · 2024Pooled it
- Mitokines as bioenergetic stress signals in cardiovascular disease: mitochondrial communication, endocrine adaptation, and translational implications.Journal of bioenergetics and biomembranes · 2026Review
- Molecular mechanism underlying the protective effects of ischemic preconditioning in total knee arthroplasty.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2025Article
- Fisetin from Dietary Supplement to a Drug Candidate: An Assessment of Potential.Current pharmaceutical biotechnology · 2025Review
- The multifaceted role of mitochondria in cardiac function: insights and approaches.Cell communication and signaling : CCS · 2024Review
- Mini-encyclopedia of mitochondria-relevant nutraceuticals protecting health in primary and secondary care-clinically relevant 3PM innovation.The EPMA journal · 2024Article
- Sonoprocessing enhances the stabilization of fisetin by encapsulation in Saccharomyces cerevisiae cells.International microbiology : the official journal of the Spanish Society for Microbiology · 2024Article
- Mitochondrial Modulators: The Defender.Biomolecules · 2023Review
- Diminished AdipoR1/APPL1 Interaction Mediates Reduced Cardioprotective Actions of Adiponectin against Myocardial Ischemia/Reperfusion Injury in Type-2 Diabetic Mice.Stem cells international · 2023Article
- Long-term administration of fisetin was not as effective as short term in ameliorating IR injury in isolated rat heart.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
According to our previous study, fisetin (3,3',4',7-tetrahydroxyflavone), a bioactive phytochemical (flavonol), reportedly showed cardioprotection against ischemia-reperfusion injury (IRI) by reducing oxidative stress and inhibiting glycogen synthase kinase 3β (GSK3β) [1]. GSK3β is said to exert a non-mitochondrial mediated cardioprotection; therefore, distinct mechanisms of GSK3β on the regulatory effect of mitochondria need to be addressed. The two distinct mitochondrial subpopulations in the heart, namely interfibrillar mitochondria (IFM) and subsarcolemmal mitochondria (SSM), respond differently to disease states. The current study aimed to understand the effect of fisetin on the subpopulation-specific preservation of IFM and SSM while rendering cardioprotection against ischemia reperfusion (I/R). Rats were pre-treated with fisetin (20 mg/kg) intraperitoneally, and IRI was induced using Langendorff isolated heart perfusion technique. Hemodynamic parameters were recorded, and the cardiac injury was assessed using infarct size (IS), lactate dehydrogenase (LDH), and creatine kinase (CK) levels. Subpopulation-specific mitochondrial preservation was evaluated by electron transport chain (ETC), catalase, superoxide dismutase (SOD), and glutathione (GSH) activities. The bioavailability of fisetin in IFM and SSM was measured using the fluorescence method. The ability of fisetin to bind directly to the mitochondrial complex-1 and activating it through donating electrons to FMN was studied using molecular docking studies and further validated by in vitro rotenone sensitivity assay. Cardioprotective effects exhibited by fisetin were mainly mediated through IFM preservation. Mitochondrial bioavailability of fisetin is more in IFM than SSM in both ex vivo and in vitro conditions. Fisetin increased mitochondrial ATP production in I/R insult hearts by activating ETC complex 1. Inhibition of complex 1 prevents the ATP-producing capacity of fisetin. Our results provide evidence that fisetin plays a protective role in myocardial IRI, possibly by preserving the functional activities of IFM.
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