Results 51 to 60 of about 49,218 (259)

Advanced glycation end products and human diseases

open access: yesJournal of Biological Research
Proteins, lipids, and nucleic acids can undergo non-enzymatic glycation and oxidation, leading to the formation of Advanced Glycation End products (AGEs).
Hamad Abu Zahra
doaj   +1 more source

NMI Regulates Adipose Adaptive Thermogenesis Through TLR4/IRF3 Signaling to Promote Obesity

open access: yesAdvanced Science, EarlyView.
Adipose tissue‐derived NMI is secreted under metabolic stress and suppresses adaptive thermogenesis through TLR4/IRF3 signaling, repressing the PPARα/PGC‐1α/UCP1 thermogenic transcriptional program. Genetic ablation or anti ‐ NMI monoclonal antibody treatment enhances energy expenditure, protects against DIO, and ameliorates adipose tissue inflammation,
Ting‐Ting Li   +7 more
wiley   +1 more source

Research Progress on Natural Products Inhibiting Advanced Glycation End Products [PDF]

open access: yesShipin Kexue
Glycation is the non-enzymatic reaction between sugars (glucose and fructose) and proteins or lipids, giving rise to the formation of advanced glycation end products (AGEs).
QI Yawei, LIU Haochi, LIU Jifeng
doaj   +1 more source

A Plant Photoregulator‐Inspired S‐Type Heterojunction System for Diabetic Keratopathy via Tri‐Modal Light‐Driven Immunometabolic Reprogramming, Tissue Repair, and Antibacterial Activity

open access: yesAdvanced Science, EarlyView.
To address the multifaceted imbalance in diabetic keratopathy, a light‐responsive biomimetic platform (WCNx‐Rh2) is developed and integrates glucose degradation, immune modulation, and antibacterial defense through a designed heterojunction and screened immunomodulator. WCNx‐Rh2 reduces AGEs/ROS and inflammatory signaling, reprogramming dendritic cells
Mengzhen Zhao   +8 more
wiley   +1 more source

Protein glycoxidation in neuropsychiatric disorders—from basic research to clinical practice

open access: yesRedox Biology
This review integrates current findings on protein glycation, glycoxidation, and carbonyl stress in selected neurodegenerative and neuropsychiatric disorders, with a particular focus on mechanistic pathways relevant to Alzheimer's disease (AD), Parkinson'
Wiktor Orlof, Mateusz Maciejczyk
doaj   +1 more source

Osseous wound repair under inhibition of the axis of advanced glycation end-products and the advanced glycation end-products receptor

open access: yesJournal of the Formosan Medical Association, 2015
Blockade of advanced glycation end-products (AGE) is able to reduce diabetic complications and control periodontitis. This study aimed to determine whether the application of aminoguanidine (AG), an AGE inhibitor, or N-phenacylthiazolium bromide (PTB ...
Sheng-Chueh Tsai   +6 more
doaj   +1 more source

S100A8/A9‐High Macrophages Activate Intestinal Fibroblasts via mCCL6/hCCL15‐CCR1 Axis to Drive Intestinal Fibrosis in Crohn's Disease

open access: yesAdvanced Science, EarlyView.
S100A8/A9‐high macrophages are markedly enriched in the stenotic intestinal tissue of patients with Crohn's disease. These profibrotic macrophages secrete mCCL6 in a STAT3‐dependent manner. mCCL6 and its human ortholog hCCL15 activate fibroblasts via the CCR1 receptor, thereby driving excessive collagen deposition.
Shu Wang   +12 more
wiley   +1 more source

Research Progress on Advanced Glycation End Products in Aging-related Diseases

open access: yesGuoji laonian yixue zazhi
Aging is an inherent physiological phenomenon that occurs throughout human life. Numerous theories have been proposed to elucidate the distinctive features of aging, encompassing oxidative stress, imbalances in protein homeostasis, deterioration of gene ...
Yanling Shen   +3 more
doaj   +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

Molecular mechanism of ischemic postconditioning in promoting diabetic ischemic brain injury repair via the microRNA‐34a–BDNF–SIX3 signaling axis

open access: yesAnimal Models and Experimental Medicine, EarlyView.
Diabetes combined with ischemic stroke (DMIS) exacerbates brain infarct size and neuronal damage compared to nondiabetic ischemic stroke (IS). This study reveals that microRNA‐34a (miR‐34a) plays a key role in DMIS pathogenesis: miR‐34a directly targets and suppresses brain‐derived neurotrophic factor (BDNF) and Sine oculis homeobox 3 (SIX3), promoting
Ling Zhao   +5 more
wiley   +1 more source

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