The Nrf-2/HO-1 Signaling Axis: A Ray of Hope in Cardiovascular Diseases

Zhang, Xueyan; Yu, Yihan; Lei, Hanyu; Cai, Yi; Shen, Jie; Zhu, Ping; He, Qing; Zhao, Mingyi

doi:10.1155/2020/5695723

Cited by 102 publications

(64 citation statements)

References 56 publications

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“…Emerging evidence has confirmed its important function in regulating ischemic heart disease, heart failure, myocardial infarction, atrial fibrillation, and myocarditis [ 42 ]. HO-1 has been extensively recognized as the downstream of Nrf-2 and plays a key role in cell adaptation to stressors through the antioxidant, antiapoptotic, and anti-inflammatory properties of its metabolic products [ 43 , 44 ]. Chen et al [ 45 ] found that polydatin protects against acute myocardial infarction-induced cardiac damage by the activation of Nrf-2/HO-1 signaling.…”

Section: Discussionmentioning

confidence: 99%

Nobiletin Attenuates Pathological Cardiac Remodeling after Myocardial Infarction via Activating PPARγ and PGC1α

et al. 2021

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Rationale. Pathological cardiac remodeling serves as a vital mechanism during the progression from myocardial infarction (MI) to chronic heart failure (CHF). Nobiletin (NOB), an active monomer extracted from the peel of citrus fruit, has been reported to have beneficial effects in cardiovascular diseases. Our study was aimed at describing the specific mechanisms through which NOB protects against pathological cardiac remodeling after MI. Materials and Methods. C57BL/6 mice were treated with coronary artery ligation to generate an MI model, followed by treatment for 3 weeks with NOB (50 mg/kg/d) or vehicle (50 mg/kg/d), with or without the peroxisome proliferator-activated receptor gamma (PPARγ) inhibitor T0070907 (1 mg/kg/d). Cardiac function (echocardiography, survival rate, Evans blue, and triphenyl tetrazolium chloride staining), fibrosis (Masson’s trichrome staining, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot (WB)), hypertrophy (haematoxylin-eosin staining, wheat germ agglutinin staining, and qRT-PCR), and apoptosis (WB and terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) staining) were evaluated. Hypoxia-induced apoptosis (TUNEL, WB) and phenylephrine- (PE-) induced pathological hypertrophy (immunofluorescence staining, qRT-PCR) models were established in primary neonatal rat ventricular myocytes (NRVMs). The effects of NOB with or without T0070907 were examined for the expression of PPARγ and PPARγ coactivator 1α (PGC1α) by WB in mice and NRVMs. The potential downstream effectors of PPARγ were further analyzed by WB in mice. Results. Following MI in mice, NOB intervention enhanced cardiac function across three predominant dimensions of pathological cardiac remodeling, which reflected in decreasing cardiac fibrosis, apoptosis, and hypertrophy decompensation. NOB intervention also alleviated apoptosis and hypertrophy in NRVMs. NOB intervention upregulated PPARγ and PGC1α in vivo and in vitro. Furthermore, the PPARγ inhibitor abolished the protective effects of NOB against pathological cardiac remodeling during the progression from MI to CHF. The potential downstream effectors of PPARγ were nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1). Conclusions. Our findings suggested that NOB alleviates pathological cardiac remodeling after MI via PPARγ and PGC1α upregulation.

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Section: Discussionmentioning

confidence: 99%

Nobiletin Attenuates Pathological Cardiac Remodeling after Myocardial Infarction via Activating PPARγ and PGC1α

et al. 2021

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“…The Nrf2driven battery of gene products also effects breakdown and/or refolding of misfolded proteins, DNA repair, mitochondrial rebuilding, autophagy regulation, as well as intracellular metabolism. Impaired Nrf2 function is a hallmark of many chronic disease conditions [150][151][152][153][154][155][156].…”

Section: Ozone Preconditioningmentioning

confidence: 99%

Ozone Preconditioning: Waking up the dragon

Thorp¹,

Thorp²

2021

The GMS

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It is said that no discovery is complete until its implications have been fully realized. The identification of a previously unrecognized phenomenon says little of its potential effects. What appears as a stroke of good luck can culminate in disaster; misfortune may harbor unimagined potential. Discovery is a double-edged sword that manifests only over time. Nowhere is this aphorism more applicable than in contemporary medical science.

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“…In the present study, exposure of Pb nanoparticles caused induction of HO‐1 gene expression. It has been reported that HO‐1 play a significant role in reducing oxidative stress 23 . One possible explanation is that since exposure to Pb nanoparticles led to HO‐1 gene expression, the cellular oxidative stress was reduced.…”

Section: Discussionmentioning

confidence: 99%

Proinflammatory response caused by lead nanoparticles triggered by engulfed nanoparticles

Shimizu

Horie

Tabei

et al. 2021

Environmental Toxicology

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In this study, the cellular effects of lead (Pb) nanoparticles with a primary particle size of 80 nm were evaluated in two types of cell lines: human lung carcinoma A549 and macrophage‐differentiated THP‐1 cells (dTHP‐1). The cellular responses induced by the Pb nanoparticles varied among the cell types. Exposure to Pb nanoparticles for 24 h at a concentration of 100 μg/ml induced interleukin‐8 (IL‐8) expression in dTHP‐1 cells. Induction of IL‐8 expression in A549 was lower than dTHP‐1 cells. Pb nanoparticles also induced the gene expression of heme oxygenase‐1 in dTHP‐1 cells but not in A549 cells. Though cellular uptake of Pb nanoparticles was observed in both the cell types, the amount of internalized Pb particles was lower in A549 cells than that in dTHP‐1 cells. Gene expression of metallothionein 2A was remarkably enhanced by Pb nanoparticle exposure in dTHP‐1 cells. Compared with Pb nanoparticles, induction of cytokines caused by lead nitrate (Pb[NO3]2), a water‐soluble Pb compound, was smaller. In conclusion, the present study revealed that Pb nanoparticles induced a stronger cellular response than Pb(NO3)2, primarily by eliciting cytokine production, in a cell type‐dependent manner.

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The Nrf-2/HO-1 Signaling Axis: A Ray of Hope in Cardiovascular Diseases

Cited by 102 publications

References 56 publications

Nobiletin Attenuates Pathological Cardiac Remodeling after Myocardial Infarction via Activating PPARγ and PGC1α

Nobiletin Attenuates Pathological Cardiac Remodeling after Myocardial Infarction via Activating PPARγ and PGC1α

Ozone Preconditioning: Waking up the dragon

Proinflammatory response caused by lead nanoparticles triggered by engulfed nanoparticles

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