Curcumin Improves Cardiopulmonary Resuscitation Outcomes by Modulating Mitochondrial Metabolism and Apoptosis in a Rat Model of Cardiac Arrest

Zhang, Jie; Liu, Siqi; Jiang, Longyuan; Hou, Jinlin; Yang, Zhengfei

doi:10.3389/fcvm.2022.908755

Cited by 3 publications

(3 citation statements)

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“…Unfortunately, there are few studies on CFLAR and CA. Apoptosis is one of the important pathologies after CA (Zhang et al 2022b), so we believe that CFLAR, as an apoptosis regulator, has the potential to improve the neurological outcome after CA.…”

Section: Discussionmentioning

confidence: 98%

Identification of predictors for neurological outcome after cardiac arrest in peripheral blood mononuclear cells through integrated bioinformatics analysis and machine learning

Qin

Liu

et al. 2023

Funct Integr Genomics

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Neurological prognostication after cardiac arrest (CA) is important to avoid pursuing futile treatments for poor outcome and inappropriate withdrawal of life-sustaining treatment for good outcome. To predict neurological outcome after CA through biomarkers in peripheral blood mononuclear cells, four datasets were downloaded from the Gene Expression Omnibus database. GSE29546 and GSE74198 were used as training datasets, while GSE92696 and GSE34643 were used as verification datasets. The intersection of differentially expressed genes and hub genes from multiscale embedded gene co-expression network analysis (MEGENA) was utilized in the machine learning screening. Key genes were identified using support vector machine recursive feature elimination (SVM-RFE), least absolute shrinkage and selection operator (LASSO) logistic regression, and random forests (RF). The results were validated using receiver operating characteristic curve analysis. An mRNA-miRNA network was constructed. The distribution of immune cells was evaluated using cell-type identification by estimating relative subsets of RNA transcripts (CIBERSORT). Five biomarkers were identified as predictors for neurological outcome after CA, with an area under the curve (AUC) greater than 0.7: CASP8 and FADD-like apoptosis regulator (CFLAR), human protein kinase X (PRKX), miR-483-5p, let-7a-5p, and let-7c-5p. Interestingly, the combination of CFLAR minus PRKX showed an even higher AUC of 0.814. The mRNA-miRNA network consisted of 30 nodes and 76 edges. Statistical differences were found in immune cell distribution, including neutrophils, NK cells active, NK cells resting, T cells CD4 memory activated, T cells CD4 memory resting, T cells CD8, B cells memory, and mast cells resting between individuals with good and poor neurological outcome after CA. In conclusion, our study identified novel predictors for neurological outcome after CA. Further clinical and laboratory studies are needed to validate our findings.

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Section: Discussionmentioning

confidence: 98%

Identification of predictors for neurological outcome after cardiac arrest in peripheral blood mononuclear cells through integrated bioinformatics analysis and machine learning

Qin

Liu

et al. 2023

Funct Integr Genomics

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“…Compared with normal mice, Ucp3 −/− mice show a deficiency in ATP production, oxygen consumption and heat production [32]. Curcumin significantly attenuates myocardial apoptosis in rat cardiomyocytes, and the expression of Ucp3 decreases, indicating that Ucp3 may be involved in curcumin-mediated mitochondrial protection [33]. Additionally, the expression of Ucp3 and Glut4 increases in lanthionine synthase C-like (LANCL1)-overexpressing L6 cells, and oxygen consumption is obviously increased [34].…”

Section: Discussionmentioning

confidence: 99%

Uncoupling Protein 3 Promotes the Myogenic Differentiation of Type IIb Myotubes in C2C12 Cells

You,

Wang,

et al. 2023

Genes

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Uncoupling protein 3 (Ucp3) is an important transporter within mitochondria and is mainly expressed in skeletal muscle, brown adipose tissue and the myocardium. However, the effects of Ucp3 on myogenic differentiation are still unclear. This study evaluated the effects of Ucp3 on myogenic differentiation, myofiber type and energy metabolism in C2C12 cells. Gain- and loss-of-function studies revealed that Ucp3 could increase the number of myotubes and promote the myogenic differentiation of C2C12 cells. Furthermore, Ucp3 promoted the expression of the type IIb myofiber marker gene myosin heavy chain 4 (Myh4) and decreased the expression of the type I myofiber marker gene myosin heavy chain 7 (Myh7). In addition, energy metabolism related to the expression of PPARG coactivator 1 alpha (Pgc1-α), ATP synthase, H+ transportation, mitochondrial F1 complex, alpha subunit 1 (Atp5a1), lactate dehydrogenase A (Ldha) and lactate dehydrogenase B (Ldhb) increased with Ucp3 overexpression. Ucp3 could promote the myogenic differentiation of type IIb myotubes and accelerate energy metabolism in C2C12 cells. This study can provide the theoretical basis for understanding the role of Ucp3 in energy metabolism.

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“…Another potential mechanism by which UCP2 may protect the myocardium against reperfusion injury is by the induction of mitophagy [ 49 ]. A high expression of UCP2 may, however, damage the heart by lowering mitochondrial membrane potential and induction of apoptosis [ 55 ]. Furthermore, UCP2 may upload the mitochondria with calcium that affects heart rhythm and energy handling [ 56 ].…”

Section: Uncoupling Proteinsmentioning

confidence: 99%

Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases

Schulz

Schlüter

2023

IJMS

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On the one hand, reactive oxygen species (ROS) are involved in the onset and progression of a wide array of diseases. On the other hand, these are a part of signaling pathways related to cell metabolism, growth and survival. While ROS are produced at various cellular sites, in cardiomyocytes the largest amount of ROS is generated by mitochondria. Apart from the electron transport chain and various other proteins, uncoupling protein (UCP) and monoamine oxidases (MAO) have been proposed to modify mitochondrial ROS formation. Here, we review the recent information on UCP and MAO in cardiac injuries induced by ischemia-reperfusion (I/R) as well as protection from I/R and heart failure secondary to I/R injury or pressure overload. The current data in the literature suggest that I/R will preferentially upregulate UCP2 in cardiac tissue but not UCP3. Studies addressing the consequences of such induction are currently inconclusive because the precise function of UCP2 in cardiac tissue is not well understood, and tissue- and species-specific aspects complicate the situation. In general, UCP2 may reduce oxidative stress by mild uncoupling and both UCP2 and UCP3 affect substrate utilization in cardiac tissue, thereby modifying post-ischemic remodeling. MAOs are important for the physiological regulation of substrate concentrations. Upon increased expression and or activity of MAOs, however, the increased production of ROS and reactive aldehydes contribute to cardiac alterations such as hypertrophy, inflammation, irreversible cardiomyocyte injury, and failure.

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Curcumin Improves Cardiopulmonary Resuscitation Outcomes by Modulating Mitochondrial Metabolism and Apoptosis in a Rat Model of Cardiac Arrest

Cited by 3 publications

References 50 publications

Identification of predictors for neurological outcome after cardiac arrest in peripheral blood mononuclear cells through integrated bioinformatics analysis and machine learning

Identification of predictors for neurological outcome after cardiac arrest in peripheral blood mononuclear cells through integrated bioinformatics analysis and machine learning

Uncoupling Protein 3 Promotes the Myogenic Differentiation of Type IIb Myotubes in C2C12 Cells

Importance of Mitochondria in Cardiac Pathologies: Focus on Uncoupling Proteins and Monoamine Oxidases

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