Advanced glycation end-products produced systemically and by macrophages: A common contributor to inflammation and degenerative diseases.
Kyunghee Byun,Yong Cheol Yoo,Myeongjoo Son,Jaesuk Lee,Goo-Bo Jeong,Young Mok Park,Ghasem Hosseini Salekdeh,Bonghee Lee +7 more
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TLDR
This review was undertaken to present, discuss, and clarify current understanding regarding AGEs formation in association with macrophages, different diseases, therapeutic and diagnostic strategy and links with RAGE inhibition.About:
This article is published in Pharmacology & Therapeutics.The article was published on 2017-09-01 and is currently open access. It has received 222 citations till now. The article focuses on the topics: RAGE (receptor).read more
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New insights into oxidative stress and inflammation during diabetes mellitus-accelerated atherosclerosis.
Ting Yuan,Ting Yang,Huan Chen,Danli Fu,Yangyang Hu,Jing Wang,Qing Yuan,Hong Yu,Wenfeng Xu,Xiang Xie +9 more
TL;DR: The consequences of the sustained increase of ROS production and inflammation that influence the acceleration of atherosclerosis by diabetes are highlighted and the potential contributions of changes in the gut microbiota and microRNA expression are discussed.
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The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality.
Jyotiska Chaudhuri,Yasmin Bains,Sanjib Guha,Arnold Kahn,David Hall,Neelanjan Bose,Neelanjan Bose,Alejandro Gugliucci,Pankaj Kapahi,Pankaj Kapahi +9 more
TL;DR: It is shown how invertebrate models, notably Drosophila melanogaster and Caenorhabditis elegans, can be used to explore AGE-related pathways in depth and to identify and assess drugs that will mitigate against the detrimental effects of AGEs-adduct development.
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Innate Immunity in the Persistent Inflammation, Immunosuppression, and Catabolism Syndrome and Its Implications for Therapy.
Hiroyuki Horiguchi,Hiroyuki Horiguchi,Tyler J. Loftus,Russell B. Hawkins,Steven L. Raymond,Julie A. Stortz,McKenzie K. Hollen,Brett P. Weiss,Elizabeth S. Miller,Azra Bihorac,Shawn D. Larson,Alicia M. Mohr,Scott C. Brakenridge,Hironori Tsujimoto,Hideki Ueno,Frederick A. Moore,Lyle L. Moldawer,Philip A. Efron +17 more
TL;DR: It is proposed that CCI and PICS after trauma or sepsis are the result of an inappropriate bone marrow response characterized by the generation of dysfunctional myeloid populations at the expense of lympho- and erythropoiesis.
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Advanced Glycation End Products (AGEs), Receptor for AGEs, Diabetes, and Bone: Review of the Literature
TL;DR: The AGE–RAGE signaling pathway has some helpful roles in the bone, including an increase in osteogenic function, and the recombinant sRAGE cannot be translated into clinical practice due to its limitations.
References
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Prostaglandins and Inflammation
TL;DR: ins biology has potential clinical relevance for atherosclerosis, the response to vascular injury and aortic aneurysm, and the roles of individual mediators and their receptors in modulating the inflammatory response.
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Advanced glycation end-products: a review.
TL;DR: The chemistry of advanced glycated end-product formation and their patho-biochemistry particularly in relation to the diabetic microvascular complications of retinopathy, neuropathy and nephropathy as well as their role in the accelerated vasculopathy observed in diabetes are discussed.
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Advanced glycation end products: sparking the development of diabetic vascular injury.
TL;DR: Because of the emerging evidence about the adverse effects of AGEs on the vasculature of patients with diabetes, a number of different therapies to inhibit A GEs are under investigation.
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RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides.
Marion A. Hofmann,Steven Drury,Caifeng Fu,Wu Qu,Akihiko Taguchi,Yan Lu,Cecilia Avila,Neeraja Kambham,Angelika Bierhaus,Peter P. Nawroth,Markus F. Neurath,Timothy Slattery,Dale L. Beach,John McClary,Mariko Nagashima,John Morser,David M. Stern,Ann Marie Schmidt +17 more
TL;DR: It is reported here that receptor for AGE (RAGE) is a central cell surface receptor for EN-RAGE (extracellular newly identified RAGE-binding protein) and related members of the S100/calgranulin superfamily.
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Aminoguanidine prevents diabetes-induced arterial wall protein cross-linking
TL;DR: The identification of aminoguanidine as an inhibitor of advanced nonenzymatic glycosylation product formation makes possible precise experimental definition of the pathogenetic significance of this process and suggests a potential clinical role for aminogsuanidine in the future treatment of chronic diabetic complications.