Uric acid aggravates myocardial ischemia–reperfusion injury via ROS/NLRP3 pyroptosis pathway

Shen, Shichun; He, Fangping; Cheng, Cheng; Xu, Bo; Sheng, Jian‐Zhong

doi:10.1016/j.biopha.2020.110990

Cited by 76 publications

(48 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Finally, a couple of years ago, some authors hypothesized that a multitarget therapy is necessary to be able to fully achieve a benefit in patients subjected to cardiac reperfusion, since AMI is a multifactorial process, wherein cardiomyocytes die through various pathways, such as apoptosis, necrosis, autophagy, and necroptosis [ 11 ], and where, with the passing of time, the list is enlarged, describing new pathways that could be triggering cell death after the reperfusion injury, such as ferroptosis [ 39 , 89 ] and pyroptosis [ 90 ]. Furthermore, not only cardiomyocytes are affected, but also other heart cell types, such as fibroblasts, immune cells, endothelial cells, and platelets [ 11 ], and targeting only one mechanism at a time may be insufficient to produce a strong and robust effect in clinical situations where many uncontrolled variables usually coexist.…”

Section: Cardioprotection By Vitamin Cmentioning

confidence: 99%

Joint Cardioprotective Effect of Vitamin C and Other Antioxidants against Reperfusion Injury in Patients with Acute Myocardial Infarction Undergoing Percutaneous Coronary Intervention

et al. 2021

View full text Add to dashboard Cite

Percutaneous coronary intervention (PCI) has long remained the gold standard therapy to restore coronary blood flow after acute myocardial infarction (AMI). However, this procedure leads to the development of increased production of reactive oxygen species (ROS) that can exacerbate the damage caused by AMI, particularly during the reperfusion phase. Numerous attempts based on antioxidant treatments, aimed to reduce the oxidative injury of cardiac tissue, have failed in achieving an effective therapy for these patients. Among these studies, results derived from the use of vitamin C (Vit C) have been inconclusive so far, likely due to suboptimal study designs, misinterpretations, and the erroneous conclusions of clinical trials. Nevertheless, recent clinical trials have shown that the intravenous infusion of Vit C prior to PCI-reduced cardiac injury biomarkers, as well as inflammatory biomarkers and ROS production. In addition, improvements of functional parameters, such as left ventricular ejection fraction (LVEF) and telediastolic left ventricular volume, showed a trend but had an inconclusive association with Vit C. Therefore, it seems reasonable that these beneficial effects could be further enhanced by the association with other antioxidant agents. Indeed, the complexity and the multifactorial nature of the mechanism of injury occurring in AMI demands multitarget agents to reach an enhancement of the expected cardioprotection, a paradigm needing to be demonstrated. The present review provides data supporting the view that an intravenous infusion containing combined safe antioxidants could be a suitable strategy to reduce cardiac injury, thus improving the clinical outcome, life quality, and life expectancy of patients subjected to PCI following AMI.

show abstract

Section: Cardioprotection By Vitamin Cmentioning

confidence: 99%

Joint Cardioprotective Effect of Vitamin C and Other Antioxidants against Reperfusion Injury in Patients with Acute Myocardial Infarction Undergoing Percutaneous Coronary Intervention

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Considering ROS as the primary cause among these stimuli, the pharmacological antagonists of accumulated succinate sufficiently ameliorated in vivo myocardial ischemia/reperfusion injury via repressing extensive ROS generation [ 29 ]. Further, uric acid aggravates MI/R-induced activation of the NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammatory cascade and pyroptosis by promoting ROS generation, while inflammasome inhibitors and ROS scavengers partly reverse the injury [ 30 ]. What is more, ROS scavenger N-acetyl cysteine (NAC) was able to reduce the amount of ROS and prevent cell death [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Dioscin Attenuates Myocardial Ischemic/Reperfusion-Induced Cardiac Dysfunction through Suppression of Reactive Oxygen Species

Lyu

Tian

Qian

et al. 2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Myocardial ischemic/reperfusion (MI/R) is a leading cause of cardiovascular disease with high morbidity and mortality. However, the mechanisms underlying pathological reperfusion remain obscure. In this study, we found that dioscin, a natural product, could be a potential candidate for treating MI/R through modulating cardiac dysfunction. Mechanistically, our work revealed that dioscin could suppress the production of reactive oxygen species (ROS) via repressing the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2) and enhancing the expression of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx). These findings indicate that dioscin may be a potential candidate for therapeutic interventions in MI/R injury.

show abstract

“…More seriously, the increased ROS levels triggers the mitochondria to produce a large amount of ROS ("oxygen triggered-oxygen release" mechanism in mitochondria) [21]. Oxidative stress can not only attack cell membrane and organelles, but also cause in ammation by interacting with in ammatory factors, further aggravating the myocardial damage caused by MI [22]. Therefore, increasing the level of antioxidant enzymes and decreasing the content of ROS are generally considered as one of the important therapeutic ideas for MI [23].…”

Section: Discussionmentioning

confidence: 99%

The Serum of MEF2D Expression in Patients with Myocardial Infarction, May be Clinical Indicators and it Mediated ROS Signaling by HDAC5

Feng

Deng

2021

Preprint

View full text Add to dashboard Cite

Objectives: In this study, we explain that the function of MEF2D gene in myocardial infarction and its possible mechanism. Methods: Patients with MI and normal volunteers were collected. The left anterior descending arteries (LAD) of mice were ligated to induce myocardial infarction. H9c2 cells were stimulated with 5% oxygen (O2) and 5% carbon dioxide (CO2) and 90% N2 for 24 h. Quantitative polymerase chain reaction (qPCR), Microarray experiments, Western blot, Enzyme-linked immunosorbent assay (ELISA) and Immunofluorescent staining were used at this experiment. Results: MEF2D mRNA and protein expressions in heart tissue of patients and mice with myocardial infarction were reduced. MEF2D protein prevented Myocardial infarction in mice of myocardial infarction. The inhibition of MEF2D aggravated Myocardial infarction in mice of myocardial infarction. MEF2D gene promoted ROS-induced oxidative stress in vitro model of myocardial infarction. MEF2D interlinkage HDAC5 to reduced oxidative stress in vivo model or vitro model. The regulation of HDAC5 adjusted the function of MEF2D in vitro model. Discussion: These data confirmed that the serum of MEF2D expression in patients with Myocardial infarction was reduced, may be clinical indicators and it inhibited ROS-induced oxidative stress signaling by HDAC5. Thus, our results suggest that targeting MEF2D may provide an approach for the treatment of myocardial infarction.

show abstract

Uric acid aggravates myocardial ischemia–reperfusion injury via ROS/NLRP3 pyroptosis pathway

Cited by 76 publications

References 44 publications

Joint Cardioprotective Effect of Vitamin C and Other Antioxidants against Reperfusion Injury in Patients with Acute Myocardial Infarction Undergoing Percutaneous Coronary Intervention

Joint Cardioprotective Effect of Vitamin C and Other Antioxidants against Reperfusion Injury in Patients with Acute Myocardial Infarction Undergoing Percutaneous Coronary Intervention

Dioscin Attenuates Myocardial Ischemic/Reperfusion-Induced Cardiac Dysfunction through Suppression of Reactive Oxygen Species

The Serum of MEF2D Expression in Patients with Myocardial Infarction, May be Clinical Indicators and it Mediated ROS Signaling by HDAC5

Contact Info

Product

Resources

About