Preventing Myocardial Injury Following Non-Cardiac Surgery: A Potential Role for Preoperative Antioxidant Therapy with Ubiquinone

Chen, Qun; Qi, Steven S.; Hocum-Stone, Laura; Lesnefsky, Edward J.; Kelly, Rosemary F.; McFalls, Edward O.

doi:10.3390/antiox10020276

Cited by 9 publications

(4 citation statements)

References 162 publications

(244 reference statements)

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“…Additionally, it may aid in immunity by controlling lysosomal and peroxisomal activity throughout the immune response (Zhao et al 2022 ). Recent clinical trials and experimental research have documented that CoQ10 consumption provides remarkable protection against acute organ injuries (including but not limited to brain, heart, lung, liver, and kidney damage) (Ali et al 2021 ; Chen et al 2021 ; Li et al 2020 ; Zhao et al 2022 ). CoQ10 is a powerful antioxidant that provides neuroprotection in some forms of neurodegenerative illness (Mancuso et al 2010 ).…”

Section: Discussionmentioning

confidence: 99%

CoQ10 targeted hippocampal ferroptosis in a status epilepticus rat model

Fikry,

Saleh,

Mahmoud

et al. 2024

Cell Tissue Res

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Status epilepticus (SE), the most severe form of epilepsy, leads to brain damage. Uncertainty persists about the mechanisms that lead to the pathophysiology of epilepsy and the death of neurons. Overloading of intracellular iron ions has recently been identified as the cause of a newly recognized form of controlled cell death called ferroptosis. Inhibiting ferroptosis has shown promise as a treatment for epilepsy, according to recent studies. So, the current study aimed to assess the possible antiepileptic impact of CoQ10 either alone or with the standard antiepileptic drug sodium valproate (SVP) and to evaluate the targeted effect of COQ10 on hippocampal oxidative stress and ferroptosis in a SE rat model. Using a lithium-pilocarpine rat model of epilepsy, we evaluated the effect of SVP, CoQ10, or both on seizure severity, histological, and immunohistochemical of the hippocampus. Furthermore, due to the essential role of oxidative stress and lipid peroxidation in inducing ferroptosis, we evaluated malonaldehyde (MDA), reduced glutathione (GSH), glutathione peroxidase 4 (GPX4), and ferritin in tissue homogenate. Our work illustrated that ferroptosis occurs in murine models of lithium-pilocarpine-induced seizures (epileptic group). Nissl staining revealed significant neurodegeneration. A significant increase in the number of astrocytes stained with an astrocyte-specific marker was observed in the hippocampus. Effective seizure relief can be achieved in the seizure model by administering CoQ10 alone compared to SVP. This was accomplished by lowering ferritin levels and increasing GPX4, reducing MDA, and increasing GSH in the hippocampus tissue homogenate. In addition, the benefits of SVP therapy for regulating iron stores, GPX4, and oxidative stress markers were amplified by incorporating CoQ10 as compared to SVP alone. It was concluded that CoQ10 alone has a more beneficial effect than SVP alone in restoring histological structures and has a targeted effect on hippocampal oxidative stress and ferroptosis. In addition, COQ10 could be useful as an adjuvant to SVP in protecting against oxidative damage and ferroptosis-related damage that result from epileptic seizures.

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Section: Discussionmentioning

confidence: 99%

CoQ10 targeted hippocampal ferroptosis in a status epilepticus rat model

Fikry,

Saleh,

Mahmoud

et al. 2024

Cell Tissue Res

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“…Troponin is not specific for myocardial ischemia or infarction, but it is the result of a broad and multifactorial dysfunction that might occur during the complex and unique perioperative period (Figure ). [63][64][65] Its elevation might merely signify worse outcome and not causation. Further research into postoperative patients with elevated troponin levels should look beyond the narrow scope of ischemia/ cardiologist consultation.…”

Section: Anesthesia and Analgesiamentioning

confidence: 99%

Pro-Con Debate: Cardiac Troponin Measurement as Part of Routine Follow-up of Myocardial Damage Following Noncardiac Surgery

Buse

Matot

2022

Anesthesia &Amp; Analgesia

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Elevated troponin levels within 3 days of surgery, independent of the presence of symptoms, are strongly linked to increased risk of short-and long-term morbidity and mortality. However, the value of screening with troponin measurements is controversial. The Canadian Cardiovascular Society guidelines on perioperative cardiac risk assessment and management for patients who undergo noncardiac surgery recommends measuring daily troponin for 48 to 72 hours after surgery in high-risk patients. Nevertheless, others doubt this recommendation, in part because postoperative elevated levels of troponin describe very little in terms of disease or event-specific pathogenesis and etiology, and thus, tailoring an intervention remains a challenge. This Pro-Con debate offers evidence-based data to stimulate physician understanding of daily practice and its significance in this matter, and assist in determining whether to use (Pro) or not to use (Con) this surveillance.

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“…Pioglitazone, a PPAR-gamma receptor agonist, increased PGC1-alpha and mitochondrial antioxidant protein expression in a porcine model of hibernating myocardium [ 74 ]. Using a similar model, administration of dietary CoQ10, a key component of the electron transport chain (ETC), has been shown to increase the expression of PGC1-alpha, enhance mitochondrial biogenesis, and reduce NT-pro BNP levels, a marker of myocardial injury [ 75 , 76 , 77 ]. These results suggest that noninvasive therapies could be used to enhance PGC1-alpha signaling and might reduce cell injury in hibernating myocardium.…”

Section: Enhanced Pgc1-alpha Signaling Improves Recovery In Hibernati...mentioning

confidence: 99%

Novel Therapeutic Approaches Enhance PGC1-alpha to Reduce Oxidant Stress-Inflammatory Signaling and Improve Functional Recovery in Hibernating Myocardium

et al. 2022

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Ischemic heart disease affects millions of people around the world. Current treatment options, including coronary artery bypass grafting, do not result in full functional recovery, highlighting the need for novel adjunctive therapeutic approaches. Hibernation describes the myocardial response to prolonged ischemia and involves a set of complex cytoprotective metabolic and functional adaptations. PGC1-alpha, a key regulator of mitochondrial energy metabolism and inhibitor of oxidant-stress-inflammatory signaling, is known to be downregulated in hibernating myocardium. PGC1-alpha is a critical component of cellular stress responses and links cellular metabolism with inflammation in the ischemic heart. While beneficial in the acute setting, a chronic state of hibernation can be associated with self-perpetuating oxidant stress-inflammatory signaling which leads to tissue injury. It is likely that incomplete functional recovery following revascularization of chronically ischemic myocardium is due to persistence of metabolic changes as well as prooxidant and proinflammatory signaling. Enhancement of PGC1-alpha signaling has been proposed as a possible way to improve functional recovery in patients with ischemic heart disease. Adjunctive mesenchymal stem cell therapy has been shown to induce PGC1-alpha signaling in hibernating myocardium and could help improve clinical outcomes for patients undergoing bypass surgery.

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Preventing Myocardial Injury Following Non-Cardiac Surgery: A Potential Role for Preoperative Antioxidant Therapy with Ubiquinone

Cited by 9 publications

References 162 publications

CoQ10 targeted hippocampal ferroptosis in a status epilepticus rat model

CoQ10 targeted hippocampal ferroptosis in a status epilepticus rat model

Pro-Con Debate: Cardiac Troponin Measurement as Part of Routine Follow-up of Myocardial Damage Following Noncardiac Surgery

Novel Therapeutic Approaches Enhance PGC1-alpha to Reduce Oxidant Stress-Inflammatory Signaling and Improve Functional Recovery in Hibernating Myocardium

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