Dietary Advanced Glycation End Products as Mediators of Obesity: Cellular and Molecular Mechanisms of Action

2021 ◽  
pp. 185-197
Author(s):  
Chinedum Ogbonnaya Eleazu ◽  
Victor Udo Nna ◽  
Joseph Bagi Suleiman ◽  
Mahaneem Mohamed
Keyword(s):  
Advanced Glycation End Products ◽  
Molecular Mechanisms ◽  
Mechanisms Of Action ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Role of Advanced Glycation End Products in Carcinogenesis and their Therapeutic Implications

2019 ◽  
Vol 24 (44) ◽  
pp. 5245-5251 ◽  
Author(s):  
David Schröter ◽  
Annika Höhn
Keyword(s):  
Advanced Glycation End Products ◽  
Molecular Mechanisms ◽  
The Body ◽  
Advanced Glycation ◽  
Therapeutic Implications ◽  
Age Related ◽  
Glycation End Products ◽  
End Products ◽  
Reduction Strategies

Aging is one of the biggest risk factors for the major prevalent diseases such as cardiovascular diseases, neurodegeneration and cancer, but due to the complex and multifactorial nature of the aging process, the molecular mechanisms underlying age-related diseases are not yet fully understood. Research has been intensive in the last years aiming to characterize the pathophysiology of aging and develop therapies to fight age-related diseases. In this context advanced glycation end products (AGEs) have received attention. AGEs, when accumulated in tissues, significantly increase the level of inflammation in the body which has long been associated with the development of cancer. Here we discuss the classical settings promoting AGE formation, as well as reduction strategies, occurrence and relevance of AGEs in cancer tissues and the role of AGE-interaction with the receptor for advanced glycation end products (RAGE) in cancer initiation and progression.

scholarly journals Advanced Glycation End Products Play Adverse Proinflammatory Activities in Osteoporosis

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Roberta Sanguineti ◽  
Alessandra Puddu ◽  
François Mach ◽  
Fabrizio Montecucco ◽  
Giorgio Luciano Viviani
Keyword(s):  
Advanced Glycation End Products ◽  
Molecular Mechanisms ◽  
Systemic Circulation ◽  
Advanced Glycation ◽  
Public Health Burden ◽  
Glycation End Products ◽  
End Products ◽  
Cross Links ◽  
High Level ◽  
Global Population

Osteoporosis is a major public health burden that is expected to further increase as the global population ages. In the last twenty years, advanced glycation end products (AGEs) have been shown to be critical mediators both in the pathogenesis and development of osteoporosis and other chronic degenerative diseases related to aging. The accumulation of AGEs within the bone induces the formation of covalent cross-links with collagen and other bone proteins which affects the mechanical properties of tissue and disturbs bone remodelling and deterioration, underlying osteoporosis. On the other hand, the gradual deterioration of the immune system during aging (defined as immunosenescence) is also characterized by the generation of a high level of oxidants and AGEs. The synthesis and accumulation of AGEs (both localized within the bone or in the systemic circulation) might trigger a vicious circle (in which inflammation and aging merged in the word “Inflammaging”) which can establish and sustain the development of osteoporosis. This narrative review will update the molecular mechanisms/pathways by which AGEs induce the functional and structural bone impairment typical of osteoporosis.

scholarly journals Receptor for Advanced Glycation End Products and Its Involvement in Inflammatory Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Yaw Kuang Chuah ◽  
Rusliza Basir ◽  
Herni Talib ◽  
Tung Hing Tie ◽  
Norshariza Nordin
Keyword(s):  
Signal Transduction ◽  
Advanced Glycation End Products ◽  
Cell Activation ◽  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Wide Spectrum ◽  
Immunoglobulin Superfamily ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

The receptor for advanced glycation end products (RAGE) is a transmembrane receptor of the immunoglobulin superfamily, capable of binding a broad repertoire of ligands. RAGE-ligands interaction induces a series of signal transduction cascades and lead to the activation of transcription factor NF-κB as well as increased expression of cytokines, chemokines, and adhesion molecules. These effects endow RAGE with the role in the signal transduction from pathogen substrates to cell activation during the onset and perpetuation of inflammation. RAGE signaling and downstream pathways have been implicated in a wide spectrum of inflammatory-related pathologic conditions such as arteriosclerosis, Alzheimer's disease, arthritis, acute respiratory failure, and sepsis. Despite the significant progress in other RAGE studies, the functional importance of the receptor in clinical situations and inflammatory diseases still remains to be fully realized. In this review, we will summarize current understandings and lines of evidence on the molecular mechanisms through which RAGE signaling contributes to the pathogenesis of the aforementioned inflammation-associated conditions.

scholarly journals Cancer Malignancy Is Enhanced by Glyceraldehyde-Derived Advanced Glycation End-Products

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Jun-Ichi Takino ◽  
Sho-Ichi Yamagishi ◽  
Masayoshi Takeuchi
Keyword(s):  
Advanced Glycation End Products ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
A549 Cells ◽  
Migration And Invasion ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Migration Capacity ◽  
Invasion Capacity

The receptor for advanced glycation end-products (RAGEs) is associated with the malignancy of cancer. A recent study has suggested that glyceraldehyde-derived AGEs (Glycer-AGEs) enhanced the malignancy of melanoma cells, but glucose-derived AGEs did not. However, the effects of Glycer-AGEs on other cancer cells remain poorly understood, and the molecular mechanisms behind the above-mentioned effect have not been clarified. The present paper aimed to examine the effect of Glycer-AGEs on cultured lung cancer A549 cells. RAGE was expressed in A549 cells. Glycer-AGEs significantly attenuated cell proliferation. Furthermore, Glycer-AGEs enhanced the migration capacity of the cells by activating Rac1viaROS and also increased their invasion capacity. We demonstrated that Glycer-AGEs enhanced the migration and invasion of A549 cells rather than their proliferation. These results suggest that Glycer-AGEs play a critical role in the malignancy of cancer rather than its proliferation and are potential targets for therapeutic intervention.

scholarly journals Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury

2021 ◽  
Author(s):  
Wiramon Rungratanawanich ◽  
Ying Qu ◽  
Xin Wang ◽  
Musthafa Mohamed Essa ◽  
Byoung-Joon Song
Keyword(s):  
Translational Research ◽  
Advanced Glycation End Products ◽  
Molecular Mechanisms ◽  
Tissue Injury ◽  
Organ Damage ◽  
Cardiovascular Complications ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
Receptor Interactions ◽  
End Products

AbstractAdvanced glycation end products (AGEs) are potentially harmful and heterogeneous molecules derived from nonenzymatic glycation. The pathological implications of AGEs are ascribed to their ability to promote oxidative stress, inflammation, and apoptosis. Recent studies in basic and translational research have revealed the contributing roles of AGEs in the development and progression of various aging-related pathological conditions, such as diabetes, cardiovascular complications, gut microbiome-associated illnesses, liver or neurodegenerative diseases, and cancer. Excessive chronic and/or acute binge consumption of alcohol (ethanol), a widely consumed addictive substance, is known to cause more than 200 diseases, including alcohol use disorder (addiction), alcoholic liver disease, and brain damage. However, despite the considerable amount of research in this area, the underlying molecular mechanisms by which alcohol abuse causes cellular toxicity and organ damage remain to be further characterized. In this review, we first briefly describe the properties of AGEs: their formation, accumulation, and receptor interactions. We then focus on the causative functions of AGEs that impact various aging-related diseases. We also highlight the biological connection of AGE–alcohol–adduct formations to alcohol-mediated tissue injury. Finally, we describe the potential translational research opportunities for treatment of various AGE- and/or alcohol-related adduct-associated disorders according to the mechanistic insights presented.

scholarly journals The Molecular Mechanism of Antioxidation of Huolisu Oral Liquid Based on Serum Analysis and Network Analysis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yihui Yin ◽  
Kai Zhang ◽  
Longyin Wei ◽  
Dongling Chen ◽  
Qian Chen ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Network Pharmacology ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Oral Liquid ◽  
Antioxidant Effects

Huolisu Oral Liquid (HLS), a well-known traditional Chinese medicine (TCM) prescription, is an over-the-counter drug that is registered and approved by the State Food and Drug Administration (Approval No. Z51020381). HLS has been widely applied in the clinical treatment of cognitive disorders and has effects on delaying aging. The antioxidant effects of HLS are closely related to its antiaging activities, but the underlying mechanisms are unclear. In this study, the potential antioxidant ingredients of HLS were screened based on serum pharmacochemistry and network pharmacology, and the potential mechanisms involved in HLS antioxidant effects were preliminarily explored. Further, the antioxidant effects of HLS were verified by in vivo and in vitro experiments. The results showed that potential antioxidant ingredients could affect the toxic advanced glycation end products-receptor for advanced glycation end products (TAGE-RAGE) signaling, mitogen-activated protein kinase (MAPK) signaling, interleukin (IL)-17 signaling, tumor necrosis factor (TNF) signaling, toll-like receptors (TLRs), cyclic adenosine monophosphate (cAMP) signaling, hypoxia-inducible factor (HIF)-1 signaling, and other related pathways by regulating GAPDH, AKT1, TP53, MAPK1, JUN, and other associated targets. Thus, HLS may reduce inflammation, control the release of inflammatory cytokines, and regulate mitochondrial autophagy and metabolic abnormalities to ultimately play an antioxidant role. This is the first study attempting to construct a multilevel network of “HLS-antioxidant targets” based on serum pharmacochemistry and network pharmacology to explore the relationship between HLS and antioxidation and the molecular mechanisms of antioxidation combined with bioinformatics functional analysis and lays a foundation for further elucidating the antioxidant mechanisms of HLS.

scholarly journals Advanced Glycation End Products: New Clinical and Molecular Perspectives

2021 ◽  
Vol 18 (14) ◽  
pp. 7236
Author(s):  
Juan Salazar ◽  
Carla Navarro ◽  
Ángel Ortega ◽  
Manuel Nava ◽  
Daniela Morillo ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Molecular Mechanisms ◽  
Measurement Techniques ◽  
First Century ◽  
Advanced Glycation ◽  
Chronic Complications ◽  
Chronic Hyperglycemia ◽  
Glycation End Products ◽  
End Products ◽  
Skin Fluorescence

Diabetes mellitus (DM) is considered one of the most massive epidemics of the twenty-first century due to its high mortality rates caused mainly due to its complications; therefore, the early identification of such complications becomes a race against time to establish a prompt diagnosis. The research of complications of DM over the years has allowed the development of numerous alternatives for diagnosis. Among these emerge the quantification of advanced glycation end products (AGEs) given their increased levels due to chronic hyperglycemia, while also being related to the induction of different stress-associated cellular responses and proinflammatory mechanisms involved in the progression of chronic complications of DM. Additionally, the investigation for more valuable and safe techniques has led to developing a newer, noninvasive, and effective tool, termed skin fluorescence (SAF). Hence, this study aimed to establish an update about the molecular mechanisms induced by AGEs during the evolution of chronic complications of DM and describe the newer measurement techniques available, highlighting SAF as a possible tool to measure the risk of developing DM chronic complications.

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