Luteolin modulates SERCA2a via Sp1 upregulation to attenuate myocardial ischemia/reperfusion injury in mice

Hu, Ya; Zhang, Chengmeng; Zhu, Hong; Wang, Shuai; Zhou, Yao; Zhao, Jiaqi; Xia, Yong; Li, Dongye

doi:10.1038/s41598-020-72325-8

Cited by 31 publications

(23 citation statements)

References 54 publications

(49 reference statements)

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“…SERCA2a plays an important role in maintaining the reuptake of this Ca 2+ . This luteolin significantly increased the SERCA2a expression in rats with an injured myocardium, which prevented contractile impairment [122]. Therefore, this study conducted proper documentation of the contribution of luteolin against doxorubicin-induced cardiotoxicity.…”

Section: Luteolinmentioning

confidence: 87%

The Role of Flavonoids as a Cardioprotective Strategy against Doxorubicin-Induced Cardiotoxicity: A Review

et al. 2022

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Doxorubicin is a widely used and promising anticancer drug; however, a severe dose-dependent cardiotoxicity hampers its therapeutic value. Doxorubicin may cause acute and chronic issues, depending on the duration of toxicity. In clinical practice, the accumulative toxic dose is up to 400 mg/m2 and increasing the dose will increase the probability of cardiac toxicity. Several molecular mechanisms underlying the pathogenesis of doxorubicin cardiotoxicity have been proposed, including oxidative stress, topoisomerase beta II inhibition, mitochondrial dysfunction, Ca2+ homeostasis dysregulation, intracellular iron accumulation, ensuing cell death (apoptosis and necrosis), autophagy, and myofibrillar disarray and loss. Natural products including flavonoids have been widely studied both in cell, animal, and human models which proves that flavonoids alleviate cardiac toxicity caused by doxorubicin. This review comprehensively summarizes cardioprotective activity flavonoids including quercetin, luteolin, rutin, apigenin, naringenin, and hesperidin against doxorubicin, both in in vitro and in vivo models.

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Section: Luteolinmentioning

confidence: 87%

The Role of Flavonoids as a Cardioprotective Strategy against Doxorubicin-Induced Cardiotoxicity: A Review

et al. 2022

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“…Furthermore, it is well known that myocardial ischemia is closely associated with morbidity and mortality of patients with coronary artery disease and acute myocardial infarction [6,7]. Nowadays, immediate restoration of cardiac blood flow supply is widely considered as a feasible clinical practice to ameliorate ischemic heart diseases; however, this intervention usually brings some unwanted side effects and would paradoxically elicit reperfusion injury [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

WITHDRAWN: Remifentanil preconditioning alleviates myocardial ischemia/reperfusion injury in rats via activating Jagged-1/Notch signaling pathway

et al. 2021

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Ischemic heart diseases have emerged as great threats to human health. Nowadays, restoration of cardiac blood flow supply is widely regarded as a feasible treatment choice for ischemic heart diseases; however, this intervention would contradictorily elicit reperfusion injury. Recently, myocardial ischemia/reperfusion injury (MI/RI) has aroused widespread public concerns. Remifentanil, an ultra-short acting opioid analgesic, is frequently used for surgical anesthesia. Previous studies have demonstrated the cardioprotective effects of remifentanil preconditioning in clinical practice and in vitro experimental models; however, its exact mechanisms remain largely unclear. This study aimed to further evaluate the protective effects of remifentanil preconditioning against MI/RI and elucidate the potential molecular mechanisms. Rat models of MI/RI were successfully established via ligation of left anterior descending coronary artery for 30 minutes and restoration of blood flow for 2 hours. Herein, animal experiments displayed that remifentanil preconditioning could alleviate myocardial damage in rat models of MI/RI. Consistently, cell model experiments implied that remifentanil preconditioning attenuated hypoxia/reoxygenation exposure-induced injury in rat cardiomyocytes. Moreover, our findings verified the involvement of Notch signaling pathway in the protective effects of remifentanil preconditioning. In addition, mechanistic studies revealed that remifentanil preconditioning could up-regulate Jagged-1 expression and that Jagged-1 mediated the cardioprotective effects of remifentanil preconditioning through activating Notch signaling pathway. Taken together, our data indicate that remifentanil preconditioning ameliorates myocardial damage in rat MI/RI models via Jagged-1-mediated Notch signaling pathway activation. Thus, this study may offer some novel clues for understanding the cardioprotective mechanisms of remifentanil preconditioning against MI/RI.

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“…It regulated gene expression by binding to gene promoters and activating the transcription of many cellular genes [23,24]. During myocardial ischemia/reperfusion, SP1 down-regulated myocardial sarco-endoplasmic reticulum Ca 2+ ATPase 2a (SERCA2a), while luteolin pretreatment increased the expression of SERCA2a and reduced MIRI by up regulating SP1 [25]. Silencing SP1 inhibited autophagy by inhibiting the expression of poly ADP-ribose polymerase-1 (PARP1), protecting cardiomyocytes from MIRI and providing a promising therapeutic target for the treatment of myocardial reperfusion injury in the future [26].…”

Section: Discussionmentioning

confidence: 99%

Construction of Potential miRNA-mRNA Regulatory Network in AMI Plasma by Bioinformatics Analysis

Yang

Gao

Meng

et al. 2022

Preprint

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Background: Acute myocardial infarction (AMI) has become the main cause of incidence rate and mortality worldwide. More and more evidences indicate that abnormally expressed microRNAs (miRNAs) are involved in the pathogenesis of AMI. However, comprehensive studies on miRNA-mRNA regulatory networks in AMI plasma are still lacking.Results: In the above three datasets, a total of 5 DEMs with downregulated expression were screened. Sp1 and EGR1 may regulate most down regulated DEM. 1074 downstream target genes were predicted. The predicted target genes of DEM were mainly enriched in PI3K/Akt signal pathway, mTOR signal pathway, Hippo signal pathway, AMPK signal pathway and HIF-1 signal pathway. By constructing DEM-hub gene network, it was found that most hub genes may be regulated by miR-142-3p, miR-375 and miR-190b. Among the top 10 hub genes, the expression of STAT3 and PTEN was consistent with that in GSE66360 dataset.Conclusion: This study constructed a potential miRNA-mRNA regulatory network in the blood of AMI for the first time, which provides a new perspective for the Pathogenesis and treatment of AMI.

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Luteolin modulates SERCA2a via Sp1 upregulation to attenuate myocardial ischemia/reperfusion injury in mice

Cited by 31 publications

References 54 publications

The Role of Flavonoids as a Cardioprotective Strategy against Doxorubicin-Induced Cardiotoxicity: A Review

The Role of Flavonoids as a Cardioprotective Strategy against Doxorubicin-Induced Cardiotoxicity: A Review

WITHDRAWN: Remifentanil preconditioning alleviates myocardial ischemia/reperfusion injury in rats via activating Jagged-1/Notch signaling pathway

Construction of Potential miRNA-mRNA Regulatory Network in AMI Plasma by Bioinformatics Analysis

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