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Glycation marker glucosepane increases with the progression of osteoarthritis and correlates with morphological and functional changes of cartilage in vivo.

This group reports a remarkable association between plasma glucosepane and osteoarthritis, with as much as a 6-fold increase in advanced human osteoarthritis compared to controls. They also report some corroborating observations in guinea pig osteoarthritis. I wonder what glycation researchers make of *plasma* glucosepane being the compartment where glucosepane was assessed. If glucosepane is formed in collagen, how does it make it into plasma? Is it simply caused by normal tissue turnover? But if so, wouldn't that mean that collagen-glucosepane could theoretically be turned over into plasma and removed or excreted from there? Maybe a kind of blood filtration/scrubber could be used to remove it?
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Dietary potassium regulates vascular calcification and arterial stiffness.

I have been pondering for years how the adequate daily intake for potassium seems so high ( up to 3.4 g/day for adult males ). The results of this study are remarkable: increased dietary potassium reduced vascular calcification and aortic stiffness, while low dietary calcium increased intracellular calcium. I wonder if the body uses calcium in place of potassium, when potassium is scarce. That vascular stiffness was altered is interesting; what implication might this have for the theory that AGE accumulation causes age-related vascular stiffness? Note that this study was done in a mutant mouse model of atherosclerosis (ApoE -/-).
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Dicarbonyls induce senescence of human vascular endothelial cells.

This was a cell culture study, so its results may not be representative of what happens in aging humans, but it seems relevant. Could GO and MGO contribute to an accumulation of senescent endothelial cells during human aging, which may more-or-less permanently effect the function of the endothelium, assuming senescent cells accumulate and do not revert to quiescent (non-senescent) cells? If so, could these senescent cells be expected to be ablated with senescent cell ablation methods? Would that fix the problems that senescent endothelial cells presumably cause?
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Advanced glycation end products (AGE) potentiates cell death in p53 negative cells via upregulaion of NF-kappa B and impairment of autophagy.

These authors mention the higher AGEs in diabetic patients, so I'm not sure whether they're talking about things like glucosepane, or something more like MG or CML. But they report in this model that AGEs appear to increase autophagy, but impair clearance of autophagosomes. This upregulates NFkB, and leads to initiation of apoptosis. I wonder whether (1) if there is an age-related increase in the AGEs that these authors tested, and (2) if so, whether this AGE-triggered induction of apoptosis may be causing age-related cell loss, contributing to changes in lysosomal function, or both.
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Skeletal Muscle Regeneration, Repair and Remodelling in Aging: The Importance of Muscle Stem Cells and Vascularization.

In this abstract, these authors note a previous publication of theirs, in which they reported a greater distance between type II fiber-associated satellite cells and capillaries in older vs. younger people. I don't recall reporting on this observation, which may be relevant for a number of topics, including the aging circulatory system, muscle function and regeneration, sarcopenia, and possibly AGEs and the ECM (if changes in these are the cause of the increased distance between satellite cells and capillaries -- just my brainstorming here).
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Advanced glycation end-products: Mechanics of aged collagen from molecule to tissue.

These researchers report on what appears to be an interesting set of observations about AGEs in the context of collagen in aged human tissue samples. They report increased spacing and decreased D-period length in both aged tissues and in their ribose model of in vitro glycation. They also found that AGEs "severely limit fiber-fiber and fibril-fibril sliding", though this was apparently only observed in the in vitro glycated tendons (apparently not from human tissue samples), so skepticism on this last bit may be appropriate.
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FACTORS ASSOCIATED WITH PENTOSIDINE ACCUMULATION IN THE HUMAN VITREOUS.

These researchers report a statistically-significant "accumulation" of the AGE pentosidine in the vitreous of the human eye with age, from 222 human vitrectomy samples. I wonder how pronounced this pentosidine accumulation is. It's also noteworthy that there was no association found between pentosidine accumulation and gender or diabetes status.
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Molecular characterization of glycation-associated skin ageing: an alternative skin model to study in vitro antiglycation activity of topical cosmeceutical and pharmaceutical formulations.

I suspect this full-thickness human skin model of glycation may be of interest to several readers on this distribution list. Here, these authors report on their development of a model of a "novel...human, reconstituted, full-thickness skin" for the purpose of "further characteriz[ation], at the molecular level, the glycation stress-driven skin ageing mechanism." They use topical aminoguanidine to help characterize the model, results themselves which may be interesting to some readers.
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