Redox signaling in aging kidney and opportunity for therapeutic intervention through natural products

Chen, Yuanyuan; Yu, Xiao; Chen, Lin; Vaziri, Nosratola D.; Ma, Shuang‐Cheng; Zhao, Ying-Yong

doi:10.1016/j.freeradbiomed.2019.06.012

Cited by 29 publications

(15 citation statements)

References 162 publications

(186 reference statements)

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“…Nicotinamide adenine dinucleotide phosphate oxidase (NOX), transforming growth factor-β (TGF-β), NF-κB and nuclear factor-erythroid 2 related factor 2 (Nrf2) are prominent mediators of oxidative stress [ 97 ], which play important roles in regulating AD development. NOX is the primary source of fibrillar Aβ-induced ROS generation, suggesting the elimination of Aβ-induced oxidative damage by inhibiting NOX may provide an attractive therapeutic target for AD treatment [ 98 ].…”

Section: The Potential Association Between Redox Signaling and Metabomentioning

confidence: 99%

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Chen

Wang²,

Wang

et al. 2020

Biomark Res

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Aging and average life expectancy have been increasing at a rapid rate, while there is an exponential risk to suffer from brain-related frailties and neurodegenerative diseases as the population ages. Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide with a projected expectation to blossom into the major challenge in elders and the cases are forecasted to increase about 3-fold in the next 40 years. Considering the etiological factors of AD are too complex to be completely understood, there is almost no effective cure to date, suggesting deeper pathomechanism insights are urgently needed. Metabolites are able to reflect the dynamic processes that are in progress or have happened, and metabolomic may therefore provide a more cost-effective and productive route to disease intervention, especially in the arena for pathomechanism exploration and new biomarker identification. In this review, we primarily focused on how redox signaling was involved in AD-related pathologies and the association between redox signaling and altered metabolic pathways. Moreover, we also expatiated the main redox signaling-associated mechanisms and their cross-talk that may be amenable to mechanism-based therapies. Five natural products with promising efficacy on AD inhibition and the benefit of AD intervention on its complications were highlighted as well. Graphical Abstract

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Section: The Potential Association Between Redox Signaling and Metabomentioning

confidence: 99%

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Chen

Wang²,

Wang

et al. 2020

Biomark Res

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“…Advanced glycation end products (AGEs) and advanced oxidation protein products (AOPPs) arise from not only chronic disease conditions such as hyperglycemia and CKD but also during aging (Vlassara et al, 2009;Frimat et al, 2017). AGEs and AOPPs mainly bind to and interact with RAGE, the receptor of AGEs, which then activates downstream pathways such as TGF-β, NF-κB, mitogen-activated protein kinase (MAPK) and NAPDH oxidase (NOX) (Zhou et al, 2012;Ott et al, 2014;Chen et al, 2019). All these mediators contribute to the induction of multiple cytokines and growth factors, eventually causing premature aging and tissue damage.…”

Section: Oxidative Stressmentioning

confidence: 99%

Cellular Senescence in Kidney Fibrosis: Pathologic Significance and Therapeutic Strategies

Zhou

Liu

2020

Front. Pharmacol.

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Age-related disorders such as chronic kidney disease (CKD) are increasingly prevalent globally and pose unprecedented challenges. In many aspects, CKD can be viewed as a state of accelerated and premature aging. Aging kidney and CKD share many common characteristic features with increased cellular senescence, a conserved program characterized by an irreversible cell cycle arrest with altered transcriptome and secretome. While developmental senescence and acute senescence may positively contribute to the fine-tuning of embryogenesis and injury repair, chronic senescence, when unresolved promptly, plays a crucial role in kidney fibrogenesis and CKD progression. Senescent cells elicit their fibrogenic actions primarily by secreting an assortment of inflammatory and profibrotic factors known as the senescence-associated secretory phenotype (SASP). Increasing evidence indicates that senescent cells could be a promising new target for therapeutic intervention known as senotherapy, which includes depleting senescent cells, modulating SASP and restoration of senescence inhibitors. In this review, we discuss current understanding of the role and mechanism of cellular senescence in kidney fibrosis. We also highlight potential options of targeting senescent cells for the treatment of CKD.

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“…Various mediators are involved in the development of CKD and may represent possible targets for therapy such as transforming growth factor (TGF)-β, nuclear factor-erythroid 2 related factor, peroxisome proliferator-activated γ receptor, IL-11 and advanced glycation endproducts 5 , 6 . Recently, studies reported involvement of miRNA in the progression of CKD progression 7 .…”

Section: Introductionmentioning

confidence: 99%

Erlotinib can halt adenine induced nephrotoxicity in mice through modulating ERK1/2, STAT3, p53 and apoptotic pathways

Awad

Saleh

Abu-Elsaad

et al. 2020

Sci Rep

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Renal fibrosis is a failed regenerative process that facilitates chronic kidney disease progression. The current study was designed to study the effect of erlotinib, a receptor tyrosine kinase inhibitor, on the progression of renal fibrosis. The study included four groups of mice: control group; adenine group: received adenine (0.2% w/w) daily with food for 4 weeks; erlotinib group: received 80 mg/ kg/day erlotinib orally (6 ml/kg/day, 1.3% w/v suspension in normal saline 0.9%) for 4 weeks; adenine + erlotinib group: received adenine and erlotinib concurrently. Kidney function and antioxidant biomarkers were measured. Renal expression of Bcl2 and p53 and histopathological changes (tubular injury and renal fibrosis) were scored. Renal tissue levels of transforming growth factor-β 1 , p-ERK1/2 and p-STAT3 were measured. Results obtained showed significant decrease (P < 0.001) in serum creatinine, urea and uric acid in erlotinib + adenine group. Level of malondialdehyde was decreased significantly (P < 0.001) while reduced glutathione and catalase levels were increased (P < 0.01) by erlotinib concurrent administration. Erlotinib markedly reduced fibrosis and tubular injury and decreased TGF-β1, p-ERK1/2 and p-STAT3 (P < 0.5). In addition, expression level of Bcl-2 was elevated (P < 0.001) while that of p53-was reduced compared to adenine alone. Erlotinib can attenuate renal fibrosis development and progression through anti-fibrotic, antioxidant and antiapoptotic pathways. Chronic kidney disease (CKD) is a global health burden and is considered as an independent risk factor for cardiovascular diseases. Its prevalence is correlated to many health problems as diabetes, hypertension and obesity 1, 2. Renal fibrosis is a failed regenerative process that facilitates the development of CKD. The progression of renal insufficiency in patients with CKD is mainly due to tubulointerstitial fibrosis, glomerular inflammation and tubular atrophy 3. Many cellular events are involved in tubulointerstitial fibrosis as infiltration of inflammatory cells, fibroblast activation, extracellular matrix (ECM) deposition and microvascular rarefaction 4. Various mediators are involved in the development of CKD and may represent possible targets for therapy such as transforming growth factor (TGF)-β, nuclear factor-erythroid 2 related factor, peroxisome proliferatoractivated γ receptor, IL-11 and advanced glycation endproducts 5, 6. Recently, studies reported involvement of miRNA in the progression of CKD progression 7. Tyrosine kinases have a pivotal role in cell signalling, and their activity deregulation can promote the development and progression of fibrotic diseases. As a result, pathologic activation of tyrosine kinases can drive fibrogenesis 8. Epidermal growth factor receptor (EGFR), a receptor tyrosine kinase, has been identified in renal tissue mainly in the epithelial cells of distal and collecting tubules, peritubular vessels and glomeruli with more abundant expression in diseased than in normal kidneys 9, 10. Activation of these r...

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Redox signaling in aging kidney and opportunity for therapeutic intervention through natural products

Cited by 29 publications

References 162 publications

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

Cellular Senescence in Kidney Fibrosis: Pathologic Significance and Therapeutic Strategies

Erlotinib can halt adenine induced nephrotoxicity in mice through modulating ERK1/2, STAT3, p53 and apoptotic pathways

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