Endogenous Secretory Receptor for Advanced Glycation End Products Protects Endothelial Cells from AGEs Induced Apoptosis

Yang, Guo-Min; Huang, Yinqiong; Wu, Xiaohong; Lin, Xiahong; Xu, Jinting; Chen, Xiaoyu; Bai, Xuefeng; Li, Qiulan

doi:10.1155/2018/8216578

Cited by 7 publications

(7 citation statements)

References 32 publications

(38 reference statements)

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“…However, a recent study that made use of a Quantitative Real Time Polymerase Chain Reaction (RT-PCR) and western blot assay provided an insight as they showed that esRAGE abrogates AGEs- mediated apoptosis and inflammation in endothelial cells by downregulating the expressions of the proapoptotic marker-Bax and inflammatory marker NF-κB while upregulating the expression of the antiapoptotic markerBcl-2 (Guomin et al, 2018).…”

Section: Esrage and Srage As Biomarkers For Rage-mediated Metabolic Ementioning

confidence: 99%

Obesity and Comorbidity: Could Simultaneous Targeting of esRAGE and sRAGE Be the Panacea?

et al. 2019

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Obesity, a chronic multifaceted disease, predisposes its patients to increased risk of metabolic disorders such as: diabetes mellitus, cardiovascular diseases, dyslipidemia, etc. Recent studies reported it to be amongst the leading causes of deaths in the world. Although several treatment options for obesity abound, many of them have not been able to successfully reverse the existing obesity and metabolic dysregulation. This has therefore warranted the need for either alternative therapies or diversification of the treatment approach for obesity and its comorbidity. When the receptor for advanced glycation end products (RAGE) interacts with its ligand, RAGE-ligand activates an inflammatory signaling cascade, that leads to the activation of nuclear factor kappa B (NF-κB) and transcription of inflammatory cytokines. This action has been associated with the development of obesity and its mediated metabolic dysregulation. In view of the increasing prevalence of obesity globally and the potential threat it places on life expectancy, this article reviewed the promising potentials of targeting endogenous secretory receptor for advanced glycation end products/soluble receptors for advanced glycation end products signaling as a treatment approach for obesity. We carried out a literature search in several electronic data bases such as: Pubmed, Pubmed Central, Google, Google Scholar, Scopus, and Medline from 1980 to 2019 to acquire the status of information concerning this. The article suggests the need for the development of an esRAGE/sRAGE targeted pharmacotherapy as a treatment approach for obesity and its comorbidity.

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Section: Esrage and Srage As Biomarkers For Rage-mediated Metabolic Ementioning

confidence: 99%

Obesity and Comorbidity: Could Simultaneous Targeting of esRAGE and sRAGE Be the Panacea?

et al. 2019

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“…Zhu et al [ 42 ] studied chicken breast and found that protein and lipid oxidation could promote AGEs formation. At the same time, endogenous AGEs are synthesized in animals, and reducing sugars in meat react spontaneously with the amino acid residues of proteins, lipids, and nucleic acids to form AGEs at a later stage [ 43 ].…”

Section: Resultsmentioning

confidence: 99%

Effect of Freeze-Thaw Cycles on the Oxidation of Protein and Fat and Its Relationship with the Formation of Heterocyclic Aromatic Amines and Advanced Glycation End Products in Raw Meat

Zhang²,

et al. 2021

Molecules

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The aim of this research was to investigate the effect of the number of freeze–thaw cycles (0, 1, 3, 5, and 7) on porcine longissimus protein and lipid oxidation, as well as changes in heterocyclic aromatic amines (HAAs) and advanced glycation end products (AGEs) and their precursors. We analyzed the relationship among HAAs, AGEs, oxidation, and precursors and found the following results after seven freeze–thaw cycles. The HAAs, Norharman and Harman, were 20.33% and 16.67% higher, respectively. The AGEs, Nε-carboxyethyllysine (CEL) and Nε-carboxymethyllysine (CML), were 11.81% and 14.02% higher, respectively. Glucose, creatine, and creatinine were reduced by 33.92%, 5.93%, and 1.12%, respectively after seven freeze–thaw cycles. Norharman was significantly correlated with thiobarbituric acid reactive substances (TBARS; r2 = 0.910) and glucose (r2 = −0.914). Harman was significantly correlated to TBARS (r2 = 0.951), carbonyl (r2 = 0.990), and glucose (r2 = −0.920). CEL was correlated to TBARS (r2 = 0.992) and carbonyl (r2 = 0.933). These changes suggest that oxidation and the Maillard reaction during freeze–thaw cycles promote HAA and AGE production in raw pork.

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“…RAGE receptors are associated with the cell membrane of most body cells and can combine with various ligands, including AGE, amphoterin, β-amyloid, S100/calgranulin [108][109][110][111][112], which results in the activation of proinflammatory pathways that play an important role in the etiopathogenesis of schizophrenia. esRAGE subtype (endogenous secretory RAGE) is an unbound form of the RAGE receptor that protects cells from the harmful effects of AGE in the mechanism of blocking RAGE activation [113]. Reduced levels of esRAGE are observed in schizophrenic patients, which consequently causes increased exposure to carbonyl stress [114].…”

Section: Glycation and Oxidative Damage In Schizophreniamentioning

confidence: 99%

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

et al. 2020

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Schizophrenia is a neurodevelopmental disorder featuring chronic, complex neuropsychiatric features. The etiology and pathogenesis of schizophrenia are not fully understood. Oxidative-antioxidant imbalance is a potential determinant of schizophrenia. Oxidative, nitrosative, or sulfuric damage to enzymes of glycolysis and tricarboxylic acid cycle, as well as calcium transport and ATP biosynthesis might cause impaired bioenergetics function in the brain. This could explain the initial symptoms, such as the first psychotic episode and mild cognitive impairment. Another concept of the etiopathogenesis of schizophrenia is associated with impaired glucose metabolism and insulin resistance with the activation of the mTOR mitochondrial pathway, which may contribute to impaired neuronal development. Consequently, cognitive processes requiring ATP are compromised and dysfunctions in synaptic transmission lead to neuronal death, preceding changes in key brain areas. This review summarizes the role and mutual interactions of oxidative damage and impaired glucose metabolism as key factors affecting metabolic complications in schizophrenia. These observations may be a premise for novel potential therapeutic targets that will delay not only the onset of first symptoms but also the progression of schizophrenia and its complications.

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Endogenous Secretory Receptor for Advanced Glycation End Products Protects Endothelial Cells from AGEs Induced Apoptosis

Cited by 7 publications

References 32 publications

Obesity and Comorbidity: Could Simultaneous Targeting of esRAGE and sRAGE Be the Panacea?

Obesity and Comorbidity: Could Simultaneous Targeting of esRAGE and sRAGE Be the Panacea?

Effect of Freeze-Thaw Cycles on the Oxidation of Protein and Fat and Its Relationship with the Formation of Heterocyclic Aromatic Amines and Advanced Glycation End Products in Raw Meat

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

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