Results 81 to 90 of about 49,140 (359)

Altered Cell-surface Receptor Levels Result from Fructose Advanced Glycation End Product-Induced Inflammation [PDF]

open access: yes, 2014
Objective: As a result of the heightened reactivity fructose demonstrates compared to glucose and our current knowledge of glucose advanced glycation end-products, the aim of this research was to further elucidate the proinflammatory pathways involved in
Blackley, Regina   +2 more
core   +1 more source

Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option? [PDF]

open access: yes, 2014
Diabetic retinopathy is one of the most important causes of blindness. The underlying mechanisms of this disease include inflammatory changes and remodeling processes of the extracellular-matrix (ECM) leading to pericyte and vascular endothelial cell ...
Chuluyan, Hector Eduardo   +3 more
core   +1 more source

Advanced glycation end products

open access: yesAtherosclerosis, 2016
Patients with peripheral artery disease (PAD) suffer from widespread atherosclerosis. Partly due to the growing awareness of cardiovascular disease, the incidence of PAD has increased considerably during the past decade. It is anticipated that algorithms to identify high risk patients for cardiovascular events require being updated, making use of novel
de Vos, Lisanne C.   +4 more
openaire   +1 more source

Advanced glycation end products, dementia, and diabetes [PDF]

open access: yesProceedings of the National Academy of Sciences, 2014
It is becoming abundantly clear that the insight into the pathological process of Alzheimer’s disease (AD) provided through autosomal dominant variants of the condition is only a partial one. The formation and aggregation of Aβ and the phosphorylation and aggregation of tau are clearly part of the core pathogenesis.
Simon, Lovestone, Ulf, Smith
openaire   +2 more sources

OTUD6A in Airway Epithelial Cells Exacerbates Allergic Asthma by Promoting Airway Inflammation and Airway Remodeling Through Deubiquitination of hResistin/mRELMα

open access: yesAdvanced Science, EarlyView.
This study elucidates a novel mechanistic role of the deubiquitinase OTUD6A in asthma pathogenesis, uncovering its regulatory function in airway inflammation and airway remodeling through the stabilization of hResistin/mRELMα. This study offers a novel regulatory axis (OTUD6A‐hResistin/mRELMα) in asthma pathogenesis and OTUD6A inhibition as a potential
Weiting Pan   +10 more
wiley   +1 more source

Protein modification and maintenance systems as biomarkers of ageing [PDF]

open access: yes, 2015
Changes in the abundance and post-translational modification of proteins and accumulation of some covalently modified proteins have been proposed to represent hallmarks of biological ageing.
Friguet, Bertrand   +7 more
core   +3 more sources

Nanozyme‐Integrated Hydrogel Targeting AGEs for Diabetic Osteoarthritis Therapy

open access: yesAdvanced Science, EarlyView.
A nanozyme–integrated hydrogel (PTC‐MP) exhibiting with mild photothermal effects is constructed, and a “3R” (restrain‐restore‐reinforce) strategy is proposed for diabetic osteoarthritis (DOA) treatment based on advanced glycation end products (AGEs) targeting.
Rui Chen   +8 more
wiley   +1 more source

Effect of AGE and Gamma-mangostin on Luteinizing Hormone Receptor (LHR) Levels in Leydig Cell Culture of Male Aging Rats: Preliminary Study

open access: yesMajalah Obat Tradisional, 2021
Advanced Glycation End Products (AGE) are proteins that can cause cell destruction by increasing oxidative stress and inflammation. This product resulted from a series of chemical reactions after an initial glycation reaction. A Leydig cell is one of the
Dicky Moch Rizal   +2 more
doaj   +1 more source

The critical role of methylglyoxal and glyoxalase 1 in diabetic nephropathy [PDF]

open access: yes, 2013
The discovery of increased formation of methylglyoxal (MG) by cell metabolism in high glucose concentration in vitro suggested possible relevance to diabetes and diabetes complications (1,2).
Rabbani, Naila, Thornalley, Paul J.
core   +1 more source

SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3

open access: yesAdvanced Science, EarlyView.
SETDB2 epigenetically represses Smad3 transcription by increasing H3K9me3 enrichment at its promoter, thereby mitigating podocyte dysfunction in DKD. The transcription factor TCF21 binds directly to the Setdb2 promoter and enhances its expression in podocytes. Abstract Podocyte dysfunction represents both an early pathological hallmark and a key driver
Lanfang Li   +14 more
wiley   +1 more source

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