Adverse Effects of Oxidative Stress on Bone and Vasculature in Corticosteroid-Associated Osteonecrosis: Potential Role of Nuclear Factor Erythroid 2-Related Factor 2 in Cytoprotection

2021 ◽  
Author(s):  
Yusuke Kubo ◽  
Wolf Drescher ◽  
Athanassios Fragoulis ◽  
Mersedeh Tohidnezhad ◽  
Holger Jahr ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adverse Effects ◽  
Potential Role ◽  
Related Factor ◽  
Nuclear Factor

scholarly journals Basic Concepts on the Role of Nuclear Factor Erythroid-Derived 2-Like 2 (Nrf2) in Age-Related Diseases

2019 ◽  
Vol 20 (13) ◽  
pp. 3208 ◽  
Author(s):  
Fabiane Valentini Francisqueti-Ferron ◽  
Artur Junio Togneri Ferron ◽  
Jéssica Leite Garcia ◽  
Carol Cristina Vágula de Almeida Silva ◽  
Mariane Róvero Costa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Transcriptional Factor ◽  
Future Research ◽  
Related Factor ◽  
Nuclear Factor ◽  
Nrf2 Pathway ◽  
Age Related ◽  
Basic Concepts

The transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) is one of the most important oxidative stress regulator in the human body. Once Nrf2 regulates the expression of a large number of cytoprotective genes, it plays a crucial role in the prevention of several diseases, including age-related disorders. However, the involvement of Nrf2 on these conditions is complex and needs to be clarified. Here, a brief compilation of the Nrf2 enrollment in the pathophysiology of the most common age-related diseases and bring insights for future research on the Nrf2 pathway is described. This review shows a controversial response of this transcriptional factor on the presented diseases. This reinforces the necessity of more studies to investigate modulation strategies for Nrf2, making it a possible therapeutic target in the treatment of age-related disorders.

scholarly journals The Role of Nrf2 in Hearing Loss

2021 ◽  
Vol 12 ◽  
Author(s):  
Dafei Li ◽  
Haiyan Zhao ◽  
Zhong-Kai Cui ◽  
Guangyong Tian
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Cell Damage ◽  
Hearing Protection ◽  
Related Factor ◽  
Nuclear Factor ◽  
The World ◽  
Hair Cell Damage ◽  
Heavy Burden

Hearing loss is a major unresolved problem in the world, which has brought a heavy burden to society, economy, and families. Hair cell damage and loss mediated by oxidative stress are considered to be important causes of hearing loss. The nuclear factor erythroid 2–related factor 2 (Nrf2) is a major regulator of antioxidant capacity and is involved in the occurrence and development of a series of toxic and chronic diseases associated with oxidative stress. In recent years, studies on the correlation between hearing loss and Nrf2 target have continuously broadened our knowledge, and Nrf2 has become a new strategic target for the development and reuse of hearing protection drugs. This review summarized the correlation of Nrf2 in various types of hearing loss, and the role of drugs in hearing protection through Nrf2 from the literature.

scholarly journals Potential Role of Nuclear FactorκB in Diabetic Cardiomyopathy

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
O. Lorenzo ◽  
B. Picatoste ◽  
S. Ares-Carrasco ◽  
E. Ramírez ◽  
J. Egido ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Diabetic Cardiomyopathy ◽  
Nuclear Factor Kappa B ◽  
Potential Role ◽  
Heart Diseases ◽  
Cardiac Injury ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa

Diabetic cardiomyopathy entails the cardiac injury induced by diabetes independently of any vascular disease or hypertension. Some transcription factors have been proposed to control the gene program involved in the setting and development of related processes. Nuclear factor-kappa B is a pleiotropic transcription factor associated to the regulation of many heart diseases. However, the nuclear factor-kappa B role in diabetic cardiomyopathy is under investigation. In this paper, we review the nuclear factor-kappa B pathway and its role in several processes that have been linked to diabetic cardiomyopathy, such as oxidative stress, inflammation, endothelial dysfunction, fibrosis, hypertrophy and apoptosis.

Sulforaphane inhibits the production of Aβ partially through activation of Nrf2-regulated Oxidative Stress

2021 ◽  
Author(s):  
Shunxi Zhang ◽  
Jia He Zhao ◽  
Zhihuai Bai ◽  
Fan Wu ◽  
Lina Luo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Potential Role ◽  
Regulation Mechanism ◽  
Related Factor ◽  
Nuclear Factor ◽  
Nrf2 Activator ◽  
Specific Symptoms

Sulforaphane (SFN), a potent nuclear factor erythroid 2-related factor 2 (Nrf2) activator, presents a very potential role in improving the Alzheimer's disease (AD)-specific symptoms. However, the regulation mechanism of SFN...

scholarly journals The Role of Nuclear Factor-E2-Related Factor 1 in the Oxidative Stress Response in MC3T3-E1 Osteoblastic Cells

2016 ◽  
Vol 31 (2) ◽  
pp. 336 ◽  
Author(s):  
So Young Park ◽  
Sung Hoon Kim ◽  
Hyun Koo Yoon ◽  
Chang Hoon Yim ◽  
Sung-Kil Lim
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Osteoblastic Cells ◽  
Related Factor ◽  
Nuclear Factor

scholarly journals Nrf2 Deficiency Exaggerates Doxorubicin-Induced Cardiotoxicity and Cardiac Dysfunction

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Siying Li ◽  
Wenjuan Wang ◽  
Ting Niu ◽  
Hui Wang ◽  
Bin Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adverse Effects ◽  
Cardiac Dysfunction ◽  
Protein Aggregates ◽  
Autophagic Flux ◽  
Related Factor ◽  
Causative Role ◽  
Myocardial Oxidative Stress ◽  
Underlying Mechanisms

The anticancer therapy of doxorubicin (Dox) has been limited by its acute and chronic cardiotoxicity. In addition to a causative role of oxidative stress, autophagy appears to play an important role in the regulation of Dox-induced cardiotoxicity. However, the underlying mechanisms remain unclear. Accordingly, we explored a role of nuclear factor erythroid-2 related factor 2 (Nrf2) in Dox-induced cardiomyopathy with a focus on myocardial oxidative stress and autophagic activity. In wild type (WT) mice, a single intraperitoneal injection of 25 mg/kg Dox rapidly induced cardiomyocyte necrosis and cardiac dysfunction, which were associated with oxidative stress, impaired autophagy, and accumulated polyubiquitinated protein aggregates. However, these Dox-induced adverse effects were exaggerated in Nrf2 knockout (Nrf2−/−) mice. In cultured cardiomyocytes, overexpression of Nrf2 increased the steady levels of LC3-II, ameliorated Dox-induced impairment of autophagic flux and accumulation of ubiquitinated protein aggregates, and suppressed Dox-induced cytotoxicity, whereas knockdown of Nrf2 exerted opposite effects. Moreover, the exaggerated adverse effects in Dox-intoxicated Nrf2 depleted cardiomyocytes were dramatically attenuated by forced activation of autophagy via overexpression of autophagy related gene 5 (Atg5). Thus, these results suggest that Nrf2 is likely an endogenous suppressor of Dox-induced cardiotoxicity by controlling both oxidative stress and autophagy in the heart.

scholarly journals Role of Nuclear Factor Erythroid 2–Related Factor 2 in the Oxidative Stress–Dependent Hypertension Associated With the Depletion of DJ-1

Hypertension ◽  
2015 ◽  
Vol 65 (6) ◽  
pp. 1251-1257 ◽  
Author(s):  
Santiago Cuevas ◽  
Yu Yang ◽  
Prasad Konkalmatt ◽  
Laureano D. Asico ◽  
Jun Feranil ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Related Factor ◽  
Nuclear Factor ◽  
Stress Dependent

scholarly journals The Taming of Nuclear Factor Erythroid-2-Related Factor-2 (Nrf2) Deglycation by Fructosamine-3-Kinase (FN3K)-Inhibitors-A Novel Strategy to Combat Cancers

Cancers ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 281
Author(s):  
Narasimha M. Beeraka ◽  
Venugopal R. Bovilla ◽  
Shalini H. Doreswamy ◽  
Sujatha Puttalingaiah ◽  
Asha Srinivasan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Cell ◽  
Advanced Glycation End Products ◽  
Signaling Cascades ◽  
Related Factor ◽  
Nuclear Factor ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Glycated stress is mediated by the advanced glycation end products (AGE) and the binding of AGEs to the receptors for advanced glycation end products (RAGEs) in cancer cells. RAGEs are involved in mediating tumorigenesis of multiple cancers through the modulation of several downstream signaling cascades. Glycated stress modulates various signaling pathways that include p38 mitogen-activated protein kinase (p38 MAPK), nuclear factor kappa–B (NF-κB), tumor necrosis factor (TNF)-α, etc., which further foster the uncontrolled proliferation, growth, metastasis, angiogenesis, drug resistance, and evasion of apoptosis in several cancers. In this review, a balanced overview on the role of glycation and deglycation in modulating several signaling cascades that are involved in the progression of cancers was discussed. Further, we have highlighted the functional role of deglycating enzyme fructosamine-3-kinase (FN3K) on Nrf2-driven cancers. The activity of FN3K is attributed to its ability to deglycate Nrf2, a master regulator of oxidative stress in cells. FN3K is a unique protein that mediates deglycation by phosphorylating basic amino acids lysine and arginine in various proteins such as Nrf2. Deglycated Nrf2 is stable and binds to small musculoaponeurotic fibrosarcoma (sMAF) proteins, thereby activating cellular antioxidant mechanisms to protect cells from oxidative stress. This cellular protection offered by Nrf2 activation, in one way, prevents the transformation of a normal cell into a cancer cell; however, in the other way, it helps a cancer cell not only to survive under hypoxic conditions but also, to stay protected from various chemo- and radio-therapeutic treatments. Therefore, the activation of Nrf2 is similar to a double-edged sword and, if not controlled properly, can lead to the development of many solid tumors. Hence, there is a need to develop novel small molecule modulators/phytochemicals that can regulate FN3K activity, thereby maintaining Nrf2 in a controlled activation state.

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