scholarly journals Skin Autofluorescence, a Novel Marker for Glycemic and Oxidative Stress-Derived Advanced Glycation Endproducts: An Overview of Current Clinical Studies, Evidence, and Limitations

2006 ◽  
Vol 8 (5) ◽  
pp. 523-535 ◽  
Author(s):  
Douwe J. Mulder ◽  
Tara Van De Water ◽  
Helen L. Lutgers ◽  
Reindert Graaff ◽  
Rijk O. Gans ◽  
...  
2012 ◽  
Vol 39 (8) ◽  
pp. 1654-1658 ◽  
Author(s):  
ANDREA K. MURRAY ◽  
TONIA L. MOORE ◽  
JOANNE B. MANNING ◽  
CHRISTOPHER E.M. GRIFFITHS ◽  
ARIANE L. HERRICK

Objective.Skin autofluorescence noninvasively assesses expression of advanced glycation endproducts and therefore potentially the presence of oxidative stress that is implicated in the pathogenesis of systemic sclerosis (SSc). We investigated whether autofluorescence was increased in patients with SSc, primary Raynaud’s phenomenon (RP), and morphea as compared to healthy controls.Methods.Measurements of autofluorescence were made at 5 upper limb sites in 16 healthy controls, 16 patients with diffuse cutaneous SSc (dcSSc), 15 with limited cutaneous SSc (lcSSc), 15 with primary RP, and 13 with morphea. For patients with morphea, additional measurements were made at the affected and an adjacent unaffected site.Results.Autofluorescence was significantly increased in patients with dcSSc but not lcSSc as compared to controls at the proximal phalanx [dcSSc median 0.15, interquartile range (IQR) 0.10–0.24, vs control 0.10, IQR 0.07–0.13; p = 0.014], dorsum of the hand (dcSSc 0.17, IQR 0.11–0.36, vs control 0.12, IQR 0.09–0.17; p = 0.031), the wrist (dcSSc 0.22, IQR 0.13–0.33, vs control 0.13, IQR 0.09–0.18; p = 0.005), and forearm (dcSSc 0.19, IQR 0.12–0.47, vs control 0.14, IQR 0.10–0.16; p = 0.022). There was a trend for autofluorescence to be increased in patients with lcSSc and at morphea sites, compared to noninvolved skin.Conclusion.Autofluorescence is increased in patients with dcSSc compared to primary RP and to healthy controls. This suggests increased oxidative stress and the potential for autofluorescence as a biomarker.


2008 ◽  
Vol 1126 (1) ◽  
pp. 276-279 ◽  
Author(s):  
Alin Stirban ◽  
Monica Negrean ◽  
Christian Götting ◽  
Jaime Uribarri ◽  
Thomas Gawlowski ◽  
...  

Heliyon ◽  
2020 ◽  
Vol 6 (11) ◽  
pp. e05364
Author(s):  
Isabella M. Atzeni ◽  
Jeltje Boersema ◽  
Hendri H. Pas ◽  
Gilles F.H. Diercks ◽  
Jean L.J.M. Scheijen ◽  
...  

2018 ◽  
Vol 25 (11) ◽  
pp. 1294-1310 ◽  
Author(s):  
Raffaella Mastrocola ◽  
Manuela Aragno ◽  
Giuseppe Alloatti ◽  
Massimo Collino ◽  
Claudia Penna ◽  
...  

In the last decades, the extension of life expectancy and the increased consumption of foods rich in saturated fats and added sugars have exposed the general population to emerging health problems. The prevalence of metabolic syndrome (MS), composed of a cluster of factors as obesity, dyslipidemia, hyperglycemia, and hypertension, is rapidly increasing in industrialized and developing countries leading to precocious onset of age-related diseases. Indeed, oxidative stress, accumulation of advanced glycation endproducts, and a chronic low-grade inflammation are common features of MS and physiological ageing. In particular, the entire set of MS factors contributes to the development of an inflammatory status named metaflammation, which has been associated with activation of early innate immune response through the assembling of the multiprotein complex inflammasome. The most investigated family of inflammasome platforms is the NOD-like receptor pyridine containing (NLRP) 3, which is activated by several exogenous and endogenous stimuli, leading to the sequential cleavage of caspase-1 and IL-1β, followed by secretion of active IL-1β. We here collect the most recent findings on NLRP3 activation in MS providing evidence of its central role in disease progression and organ dysfunction in target tissues of metaflammation, in particular in cardiovascular, hepatic and renal complications, with a focus on oxidative stress and advanced glycation endproducts. A wide overview of the most promising strategies for the modulation of NLRP3 activation and related metabolic repercussions is also provided, since the finding of specific pharmacological tools is an urgent requirement to reduce the social and economic burden of MS- and elderly-associated diseases.


2007 ◽  
Vol 193 (2) ◽  
pp. 269-277 ◽  
Author(s):  
Martha Lappas ◽  
Michael Permezel ◽  
Gregory E Rice

Processes of human labour include increased oxidative stress, formation of inflammatory mediators (e.g. cytokines) and uterotonic phospholipid metabolites (e.g. prostaglandins). In non-gestational tissues, advanced glycation endproducts (AGE) induce the expression of pro-inflammatory molecules through mitogen-activated protein kinase and nuclear factor κB (NF-κB)-dependent pathways. Thus, the aim of this study was to investigate the effects of AGE on 8-isoprostane (a marker of oxidative stress), pro-inflammatory cytokine and prostaglandin release in human gestational tissues, and to define the signalling pathways involved. Human placenta and gestational membranes (amnion and choriodecidua combined; n=5) were incubated in the absence or presence of AGE–BSA (0.25, 0.5, 1 and 2 mg/ml) for 18 h. AGE significantly increased in vitro release of tumour necrosis factor-α, interleukin (IL)-1β, IL-6, IL-8, prostaglandin (PG)E2, PGF2α and 8-isoprostane from human placenta and gestational membranes. This was associated with a concomitant increase in NF-κB p65 activation and ERK 1/2 phosphorylation. AGE-stimulated 8-isoprostane, cytokine and prostaglandin production was significantly suppressed by the ERK 1/2 inhibitor U0126 and the NF-κB inhibitor BAY 11-7082. In conclusion, AGE mediates inflammatory actions in human gestational tissues. Protein kinases and the NF-κB pathway play an essential role in AGE signalling in human gestational tissues.


Bone ◽  
2007 ◽  
Vol 41 (6) ◽  
pp. S2-S3
Author(s):  
AD McCarthy ◽  
C Sedlinsky ◽  
AM Cortizo ◽  
L Bruzzone ◽  
V Arnol ◽  
...  

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