Nrf2 for a key member of redox regulation: A novel insight against myocardial ischemia and reperfusion injuries

Han, Xuejie; Wang, Hongxia; Du, Fenghe; Zeng, Xiangjun; Guo, Caixia

doi:10.1016/j.biopha.2023.115855

Cited by 5 publications

(3 citation statements)

References 201 publications

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“…GSH, a major constituent of the non-enzymatic antioxidant system, plays a crucial role in cellular redox balance by scavenging various forms of ROS and reactive nitrogen species (RNS) (Bansal & Simon, 2018;Georgiou-Siafis & Tsiftsoglou, 2023;Kennedy et al, 2020). NRF2 is a major antioxidant transcription factor that plays a key role in regulating redox signalling to maintain redox homeostasis and is involved in a variety of cellular processes (Han et al, 2023;Park et al, 2023;Yang & Smith, 2023). Our results…”

Section: Discussionmentioning

confidence: 59%

Enhancing antioxidant levels and mitochondrial function in porcine oocyte maturation and embryonic development through notoginsenoside R1 supplementation

He,

Liu,

Huang

et al. 2024

Reprod Domestic Animals

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This study examines the impact of Notoginsenoside R1 (NGR1), a compound from Panax notoginseng, on the maturation of porcine oocytes and their embryonic development, focusing on its effects on antioxidant levels and mitochondrial function. This study demonstrates that supplementing in vitro maturation (IVM) medium with NGR1 significantly enhances several biochemical parameters. These include elevated levels of glutathione (GSH), nuclear factor erythrocyte 2‐related factor 2 (NRF2) and mRNA expression of catalase (CAT) and GPX. Concurrently, we observed a decrease in reactive oxygen species (ROS) levels and an increase in JC‐1 immunofluorescence, mitochondrial distribution, peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC1α) and nuclear NRF2 mRNA levels. Additionally, there was an increase in ATP production and lipid droplets (LDs) immunofluorescence. These biochemical improvements correlate with enhanced embryonic outcomes, including a higher blastocyst rate, increased total cell count, enhanced proliferative capacity and elevated octamer‐binding transcription factor 4 (Oct4) and superoxide dismutase 2 (Sod2) gene expression. Furthermore, NGR1 supplementation resulted in decreased apoptosis, reduced caspase 3 (Cas3) and BCL2‐Associated X (Bax) mRNA levels and decreased glucose‐regulated protein 78 kD (GRP78) immunofluorescence in porcine oocytes undergoing in vitro maturation. These findings suggest that NGR1 plays a crucial role in promoting porcine oocyte maturation and subsequent embryonic development by providing antioxidant levels and mitochondrial protection.

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Section: Discussionmentioning

confidence: 59%

Enhancing antioxidant levels and mitochondrial function in porcine oocyte maturation and embryonic development through notoginsenoside R1 supplementation

He,

Liu,

Huang

et al. 2024

Reprod Domestic Animals

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“…The main regulator of cellular redox balance is the transcription factor NF-E2-related factor 2 (Nrf2), which inhibits oxidative stress, inflammation, and apoptosis (Han et al, 2023). Cu-induced oxidative stress stimulated Nrf2 recruitment to the peroxisome proliferators-activated receptor γ (PPARγ) promoter, inducing transcription of the target gene and subsequent lipogenesis (Zhong et al, 2022).…”

Section: Oxidative Stress and Antioxidant Capacity Of Cumentioning

confidence: 99%

Copper homeostasis dysregulation in respiratory diseases: a review of current knowledge

Song,

Yue,

Zhang

et al. 2024

Front. Physiol.

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Cu is an essential micronutrient for various physiological processes in almost all human cell types. Given the critical role of Cu in a wide range of cellular processes, the local concentrations of Cu and the cellular distribution of Cu transporter proteins in the lung are essential for maintaining a steady-state internal environment. Dysfunctional Cu metabolism or regulatory pathways can lead to an imbalance in Cu homeostasis in the lungs, affecting both acute and chronic pathological processes. Recent studies have identified a new form of Cu-dependent cell death called cuproptosis, which has generated renewed interest in the role of Cu homeostasis in diseases. Cuproptosis differs from other known cell death pathways. This occurs through the direct binding of Cu ions to lipoylated components of the tricarboxylic acid cycle during mitochondrial respiration, leading to the aggregation of lipoylated proteins and the subsequent downregulation of Fe-S cluster proteins, which causes toxic stress to the proteins and ultimately leads to cell death. Here, we discuss the impact of dysregulated Cu homeostasis on the pathogenesis of various respiratory diseases, including asthma, chronic obstructive pulmonary disease, idiopathic interstitial fibrosis, and lung cancer. We also discuss the therapeutic potential of targeting Cu. This study highlights the intricate interplay between copper, cellular processes, and respiratory health. Copper, while essential, must be carefully regulated to maintain the delicate balance between necessity and toxicity in living organisms. This review highlights the need to further investigate the precise mechanisms of copper interactions with infections and immune inflammation in the context of respiratory diseases and explore the potential of therapeutic strategies for copper, cuproptosis, and other related effects.

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“… 18 Thus, the aforementioned studies have confirmed the involvement of Nrf2/HO‐1 in the occurrence and progression of MIRI. 19 However, the involvement of Nrf2 and ferroptosis in cardiac microvascular function during MIRI remains unclear, necessitating urgent investigation.…”

Section: Introductionmentioning

confidence: 99%

PEDF and 34‐mer peptide inhibit cardiac microvascular endothelial cell ferroptosis via Nrf2/HO‐1 signalling in myocardial ischemia‐reperfusion injury

Lu,

Qi,

et al. 2024

J Cellular Molecular Medi

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Myocardial ischemia‐reperfusion injury (MIRI) represents a critical pathology in acute myocardial infarction (AMI), which is characterized by high mortality and morbidity. Cardiac microvascular dysfunction contributes to MIRI, potentially culminating in heart failure (HF). Pigment epithelium‐derived factor (PEDF), which belongs to the non‐inhibitory serpin family, exhibits several physiological effects, including anti‐angiogenesis, anti‐inflammatory and antioxidant properties. Our study aims to explore the impact of PEDF and its functional peptide 34‐mer on both cardiac microvascular perfusion in MIRI rats and human cardiac microvascular endothelial cells (HCMECs) injury under hypoxia reoxygenation (HR). It has been shown that MIRI is accompanied by ferroptosis in HCMECs. Furthermore, we investigated the effect of PEDF and its 34‐mer, particularly regarding the Nrf2/HO‐1 signalling pathway. Our results demonstrated that PEDF 34‐mer significantly ameliorated cardiac microvascular dysfunction following MIRI. Additionally, they exhibited a notable suppression of ferroptosis in HCMECs, and these effects were mediated through activation of Nrf2/HO‐1 signalling. These findings highlight the therapeutic potential of PEDF and 34‐mer in alleviating microvascular dysfunction and MIRI. By enhancing cardiac microvascular perfusion and mitigating endothelial ferroptosis, PEDF and its derivative peptide represent promising candidates for the treatment of AMI.

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Nrf2 for a key member of redox regulation: A novel insight against myocardial ischemia and reperfusion injuries

Cited by 5 publications

References 201 publications

Enhancing antioxidant levels and mitochondrial function in porcine oocyte maturation and embryonic development through notoginsenoside R1 supplementation

Enhancing antioxidant levels and mitochondrial function in porcine oocyte maturation and embryonic development through notoginsenoside R1 supplementation

Copper homeostasis dysregulation in respiratory diseases: a review of current knowledge

PEDF and 34‐mer peptide inhibit cardiac microvascular endothelial cell ferroptosis via Nrf2/HO‐1 signalling in myocardial ischemia‐reperfusion injury

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