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Article ; Online: The use of the soluble receptor for advanced glycation-end products (sRAGE) as a potential biomarker of disease risk and adverse outcomes.

Erusalimsky, Jorge D

2021 Volume 42, Page(s) 101958

Abstract: The soluble receptor for advanced glycation end-products (sRAGE) has been classically considered a sink for pro-inflammatory RAGE ligands and as such has been associated with protection from inflammatory stress and disease. An alternative, though not ... ...

Abstract	The soluble receptor for advanced glycation end-products (sRAGE) has been classically considered a sink for pro-inflammatory RAGE ligands and as such has been associated with protection from inflammatory stress and disease. An alternative, though not mutually exclusive view is that high levels of sRAGE in circulation reflect the overstimulation of cell surface RAGE which if persistent, lead to the amplification of pro-inflammatory processes and the exacerbation of pathological states. With these two scenarios in mind this review focuses on the potential role of sRAGE as a prospective biomarker of disease risk and adverse outcomes.
MeSH term(s)	Biomarkers ; Disease ; Glycation End Products, Advanced ; Humans ; Prospective Studies ; Receptor for Advanced Glycation End Products
Chemical Substances	Biomarkers ; Glycation End Products, Advanced ; Receptor for Advanced Glycation End Products
Language	English
Publishing date	2021-03-29
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2021.101958
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Article ; Online: Oxidative stress, telomeres and cellular senescence: What non-drug interventions might break the link?

Erusalimsky, Jorge D

Free radical biology & medicine

2020 Volume 150, Page(s) 87–95

Abstract: Telomeres are higher order structures that cap and protect chromosome ends. Telomeric DNA naturally shortens during somatic cell division and as a result of oxidative stress. Excessive shortening disrupts the integrity of the telomere, causing cellular ... ...

Abstract	Telomeres are higher order structures that cap and protect chromosome ends. Telomeric DNA naturally shortens during somatic cell division and as a result of oxidative stress. Excessive shortening disrupts the integrity of the telomere, causing cellular senescence, one of the hallmarks of organismal ageing. The accumulation of senescent cells with ageing contributes to the loss of tissue homeostasis and the development of age-related pathologies. Hence, counteracting telomere shortening may be one relevant approach to develop strategies for healthier ageing. In this review I present the case for the existence of a link between oxidative stress, accelerated telomere shortening and cellular senescence. I also examine findings from human observational studies exploring associations between telomere length and oxidative stress-related parameters. Finally, I discuss results from randomised control trials testing the impact of non-pharmacological lifestyle interventions on the maintenance of telomere length, considering the potential mechanisms that might be involved.
MeSH term(s)	Aging/genetics ; Cellular Senescence ; Humans ; Oxidative Stress ; Telomere/genetics ; Telomere Shortening
Language	English
Publishing date	2020-02-13
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2020.02.008
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Article ; Online: The use of the soluble receptor for advanced glycation-end products (sRAGE) as a potential biomarker of disease risk and adverse outcomes

Jorge D. Erusalimsky

Redox Biology, Vol 42, Iss , Pp 101958- (2021)

2021

Abstract	The soluble receptor for advanced glycation end-products (sRAGE) has been classically considered a sink for pro-inflammatory RAGE ligands and as such has been associated with protection from inflammatory stress and disease. An alternative, though not mutually exclusive view is that high levels of sRAGE in circulation reflect the overstimulation of cell surface RAGE which if persistent, lead to the amplification of pro-inflammatory processes and the exacerbation of pathological states. With these two scenarios in mind this review focuses on the potential role of sRAGE as a prospective biomarker of disease risk and adverse outcomes.
Keywords	Biomarker ; Cardiovascular disease ; Disease risk ; Inflammation ; Frailty ; Mortality ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Frailty Influences the Relationship between the Soluble Receptor for Advanced Glycation-End Products and Mortality in Older Adults with Diabetes Mellitus.

Butcher, Lee / Carnicero, Jose A / Pérès, Karine / Bandinelli, Stefania / García-García, Francisco Jose / Rodriguez-Artalejo, Fernando / Rodriguez-Mañas, Leocadio / Erusalimsky, Jorge D

Gerontology

2024 , Page(s) 1–10

Abstract: Introduction: Frailty is prevalent among older adults with diabetes mellitus. Elevated serum levels of the soluble receptor for advanced glycation-end products (sRAGE) predict mortality in frail older adults. The evidence that sRAGE is also related to ... ...

Abstract	Introduction: Frailty is prevalent among older adults with diabetes mellitus. Elevated serum levels of the soluble receptor for advanced glycation-end products (sRAGE) predict mortality in frail older adults. The evidence that sRAGE is also related to higher mortality in older adults with diabetes mellitus is inconsistent. Therefore, this study explored if frailty status influences the relationship between sRAGE and mortality in older adults with this condition. Methods: We analysed data of 391 participants with diabetes mellitus (median age, 76 years) from four European cohorts enrolled in the FRAILOMIC project. Frailty was evaluated at baseline using Fried's criteria. Serum sRAGE was determined by ELISA. Participants were stratified by frailty status (n = 280 non-frail and 111 frail). Multivariate Cox proportional hazards regression and Kaplan-Meier survival analysis were used to assess the relationship between sRAGE and mortality. Results: During 6 years of follow-up, 98 participants died (46 non-frail and 52 frail). Non-survivors had significantly higher baseline levels of sRAGE than survivors (median [IQR]: 1,392 [962-2,043] pg/mL vs. 1,212 [963-1,514], p = 0.008). High serum sRAGE (>1,617 pg/mL) was associated with increased mortality in the whole diabetes sample after adjustment for relevant confounders (HR 2.06, 95% CI: 1.36-3.11, p < 0.001), and there was an interaction between sRAGE and frailty (p = 0.006). Accordingly, the association between sRAGE and mortality was stronger in the frail group compared to the non-frail group (HR 2.52, 95% CI: 1.30-4.90, p = 0.006 vs. HR 1.71, 95% CI: 0.91-3.23, p = 0.099, respectively). Likewise, Kaplan-Meier curves showed a significant difference in survival rates between frail participants with high sRAGE and those with low sRAGE (p = 0.001), whereas no survival difference was seen in the non-frail group (p = 0.09). Conclusions: Frailty status influences the relationship between sRAGE and mortality in older adults with diabetes mellitus. Determination of sRAGE in this population could be a useful tool for risk stratification.
Language	English
Publishing date	2024-04-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	193798-4
ISSN	1423-0003 ; 0304-324X
ISSN (online)	1423-0003
ISSN	0304-324X
DOI	10.1159/000538292
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Article: Vascular endothelial senescence: from mechanisms to pathophysiology.

Erusalimsky, Jorge D

Journal of applied physiology (Bethesda, Md. : 1985)

2008 Volume 106, Issue 1, Page(s) 326–332

Abstract: Most mitotically competent mammalian cell types can react to stress by undergoing a phenotypically distinctive and permanent form of growth arrest called "cellular senescence." This response has been extensively characterized in cell culture and more ... ...

Abstract	Most mitotically competent mammalian cell types can react to stress by undergoing a phenotypically distinctive and permanent form of growth arrest called "cellular senescence." This response has been extensively characterized in cell culture and more recently it has been found to occur also in vivo in a number of tissues. In this review I will present the case for the occurrence of senescence in the vascular endothelium. I will also discuss the mechanisms and factors that modulate endothelial cell replicative capacity and the onset of senescence. Finally, I will examine the senescent phenotype and its possible consequences for the development and progression of vascular diseases.
MeSH term(s)	Animals ; Apoptosis ; Atherosclerosis/pathology ; Cell Proliferation ; Cellular Senescence ; DNA Damage ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Endothelium, Vascular/physiopathology ; Humans ; Mitochondria/pathology ; Neovascularization, Physiologic ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Telomerase/metabolism ; Telomere/metabolism ; Thrombosis/pathology ; Vasodilation
Chemical Substances	Reactive Oxygen Species ; Telomerase (EC 2.7.7.49)
Language	English
Publishing date	2008-11-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	219139-8
ISSN	1522-1601 ; 8750-7587 ; 0021-8987 ; 0161-7567
ISSN (online)	1522-1601
ISSN	8750-7587 ; 0021-8987 ; 0161-7567
DOI	10.1152/japplphysiol.91353.2008
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Article ; Online: DPP4 Promotes Human Endothelial Cell Senescence and Dysfunction via the PAR2-COX-2-TP Axis and NLRP3 Inflammasome Activation.

Valencia, Inés / Vallejo, Susana / Dongil, Pilar / Romero, Alejandra / San Hipólito-Luengo, Álvaro / Shamoon, Licia / Posada, María / García-Olmo, Damián / Carraro, Raffaelle / Erusalimsky, Jorge D / Romacho, Tania / Peiró, Concepción / Sánchez-Ferrer, Carlos F

Hypertension (Dallas, Tex. : 1979)

2022 Volume 79, Issue 7, Page(s) 1361–1373

Abstract: Background: Abnormal accumulation of senescent cells in the vessel wall leads to a compromised vascular function contributing to vascular aging. Soluble DPP4 (dipeptidyl peptidase 4; sDPP4) secretion from visceral adipose tissue is enhanced in obesity, ... ...

Abstract	Background: Abnormal accumulation of senescent cells in the vessel wall leads to a compromised vascular function contributing to vascular aging. Soluble DPP4 (dipeptidyl peptidase 4; sDPP4) secretion from visceral adipose tissue is enhanced in obesity, now considered a progeric condition. sDPP4 triggers vascular deleterious effects, albeit its contribution to vascular aging is unknown. We aimed to explore sDPP4 involvement in vascular aging, unraveling the molecular pathway by which sDPP4 acts on the endothelium. Methods: Human endothelial cell senescence was assessed by senescence-associated β-galactosidase assay, visualization of DNA damage, and expression of prosenescent markers, whereas vascular function was evaluated by myography over human dissected microvessels. In visceral adipose tissue biopsies from a cohort of obese patients, we explored several age-related parameters in vitro and ex vivo. Results: By a common mechanism, sDPP4 triggers endothelial cell senescence and endothelial dysfunction in isolated human resistance arteries. sDPP4 activates the metabotropic receptor PAR2 (protease-activated receptor 2), COX-2 (cyclooxygenase 2) activity, and the production of TXA Conclusions: These results reveal sDPP4 as a relevant mediator in early vascular aging and highlight its capacity activating main proinflammatory mediators in the endothelium that might be pharmacologically tackled.
MeSH term(s)	Biomarkers/metabolism ; Cellular Senescence ; Cyclooxygenase 2/genetics ; Cyclooxygenase 2/metabolism ; Dipeptidyl Peptidase 4/metabolism ; Endothelial Cells/metabolism ; Humans ; Inflammasomes/metabolism ; Inflammasomes/pharmacology ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Obesity/metabolism ; Receptor, PAR-2/genetics ; Receptor, PAR-2/metabolism ; Receptors, Thromboxane/genetics ; Receptors, Thromboxane/metabolism
Chemical Substances	Biomarkers ; F2RL1 protein, human ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; NLRP3 protein, human ; Receptor, PAR-2 ; Receptors, Thromboxane ; Cyclooxygenase 2 (EC 1.14.99.1) ; PTGS2 protein, human (EC 1.14.99.1) ; DPP4 protein, human (EC 3.4.14.5) ; Dipeptidyl Peptidase 4 (EC 3.4.14.5)
Language	English
Publishing date	2022-04-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.121.18477
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Article ; Online: High levels of soluble RAGE are associated with a greater risk of mortality in COVID-19 patients treated with dexamethasone.

Butcher, Lee / Zaldua, Jun-Cezar / Carnicero, Jose A / Hawkins, Karl / Whitley, Janet / Mothukuri, Rangaswamy / Evans, Phillip A / Morris, Keith / Pillai, Suresh / Erusalimsky, Jorge D

Respiratory research

2022 Volume 23, Issue 1, Page(s) 303

Abstract: Blood levels of the soluble receptor for advanced glycation end-products (sRAGE) are acutely elevated during the host inflammatory response to infection and predict mortality in COVID-19. However, the prognostic performance of this biomarker in the ... ...

Abstract	Blood levels of the soluble receptor for advanced glycation end-products (sRAGE) are acutely elevated during the host inflammatory response to infection and predict mortality in COVID-19. However, the prognostic performance of this biomarker in the context of treatments to reduce inflammation is unclear. In this study we investigated the association between sRAGE and mortality in dexamethasone-treated COVID-19 patients. We studied 89 SARS-CoV-2 positive subjects and 22 controls attending the emergency department of a University Teaching Hospital during the second wave of COVID-19 and measured sRAGE at admission. In positive individuals sRAGE increased with disease severity and correlated with the National Early Warning Score 2 (Pearson's r = 0.56, p < 0.001). Fourteen out of 72 patients treated with dexamethasone died during 28 days of follow-up. Survival rates were significantly lower in patients with high sRAGE (> 3532 pg/mL) than in those with low sRAGE (p = 0.01). Higher sRAGE levels were associated with an increased risk of death after adjustment for relevant covariates. In contrast, IL-6 did not predict mortality in these patients. These results demonstrate that sRAGE remains an independent predictor of mortality among COVID-19 patients treated with dexamethasone. Determination of sRAGE could be useful for the clinical management of this patient population.
MeSH term(s)	Humans ; Receptor for Advanced Glycation End Products ; COVID-19/drug therapy ; SARS-CoV-2 ; Biomarkers ; Dexamethasone/therapeutic use ; Glycation End Products, Advanced
Chemical Substances	Receptor for Advanced Glycation End Products ; Biomarkers ; Dexamethasone (7S5I7G3JQL) ; Glycation End Products, Advanced
Language	English
Publishing date	2022-11-05
Publishing country	England
Document type	Letter
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-993X
ISSN (online)	1465-993X
ISSN	1465-993X
DOI	10.1186/s12931-022-02220-5
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Article ; Online: Higher sRAGE Levels Predict Mortality in Frail Older Adults with Cardiovascular Disease.

Butcher, Lee / Carnicero, Jose Antonio / Pérès, Karine / Colpo, Marco / Gomez Cabrero, David / Dartigues, Jean-François / Bandinelli, Stefania / Garcia-Garcia, Francisco Jose / Rodríguez-Mañas, Leocadio / Erusalimsky, Jorge D

Gerontology

2021 Volume 67, Issue 2, Page(s) 202–210

Abstract: Introduction: The evidence that blood levels of the soluble receptor for advanced glycation end products (sRAGE) predict mortality in people with cardiovascular diseases (CVD) is inconsistent. To clarify this matter, we investigated if frailty status ... ...

Abstract	Introduction: The evidence that blood levels of the soluble receptor for advanced glycation end products (sRAGE) predict mortality in people with cardiovascular diseases (CVD) is inconsistent. To clarify this matter, we investigated if frailty status influences this association. Methods: We analysed data of 1,016 individuals (median age, 75 years) from 3 population-based European cohorts, enrolled in the FRAILOMIC project. Participants were stratified by history of CVD and frailty status. Mortality was recorded during 8 years of follow-up. Results: In adjusted Cox regression models, baseline serum sRAGE was positively associated with an increased risk of mortality in participants with CVD (HR 1.64, 95% CI 1.09-2.49, p = 0.019) but not in non-CVD. Within the CVD group, the risk of death was markedly enhanced in the frail subgroup (CVD-F, HR 1.97, 95% CI 1.18-3.29, p = 0.009), compared to the non-frail subgroup (CVD-NF, HR 1.50, 95% CI 0.71-3.15, p = 0.287). Kaplan-Meier analysis showed that the median survival time of CVD-F with high sRAGE (>1,554 pg/mL) was 2.9 years shorter than that of CVD-F with low sRAGE, whereas no survival difference was seen for CVD-NF. Area under the ROC curve analysis demonstrated that for CVD-F, addition of sRAGE to the prediction model increased its prognostic value. Conclusions: Frailty status influences the relationship between sRAGE and mortality in older adults with CVD. sRAGE could be used as a prognostic marker of mortality for these individuals, particularly if they are also frail.
MeSH term(s)	Aged ; Biomarkers ; Cardiovascular Diseases ; Frail Elderly ; Humans ; Proportional Hazards Models ; Receptor for Advanced Glycation End Products
Chemical Substances	Biomarkers ; Receptor for Advanced Glycation End Products
Language	English
Publishing date	2021-01-21
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	193798-4
ISSN	1423-0003 ; 0304-324X
ISSN (online)	1423-0003
ISSN	0304-324X
DOI	10.1159/000512287
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Article ; Online: The Longitudinal Relationship Between Cortisol Responses to Mental Stress and Leukocyte Telomere Attrition.

Steptoe, Andrew / Hamer, Mark / Lin, Jue / Blackburn, Elizabeth H / Erusalimsky, Jorge D

The Journal of clinical endocrinology and metabolism

2017 Volume 102, Issue 3, Page(s) 962–969

Abstract: Context: Chronic psychological stress has been associated with shorter telomeres, but the underlying mechanisms are poorly understood. One possibility is that the neuroendocrine responses to stress exposure are involved.: Objective: To test the ... ...

Abstract	Context: Chronic psychological stress has been associated with shorter telomeres, but the underlying mechanisms are poorly understood. One possibility is that the neuroendocrine responses to stress exposure are involved. Objective: To test the hypothesis that greater cortisol responsivity to acute stressors predicts more rapid telomere attrition. Design: We measured salivary cortisol responses to 2 challenging behavioral tasks. Leukocyte telomere length was measured at the time of mental stress testing and 3 years later. Participants: We studied 411 initially healthy men and women aged 54 to 76 years. Main outcome measure: Leukocyte telomere length. Results: Cortisol responses to this protocol were small; we divided participants into cortisol responders (n = 156) and nonresponders (n = 255) using a criterion (≥20% increase in cortisol concentration) previously shown to predict increases in cardiovascular disease risk. There was no significant association between cortisol responsivity and baseline telomere length, although cortisol responders tended to have somewhat shorter telomeres (β = -0.061; standard error, 0.049). But cortisol responders had shorter telomeres and more rapid telomere attrition than nonresponders on follow-up, after controlling statistically for age, sex, socioeconomic status, smoking, time of day of stress , and baseline telomere length (β = -0.10; standard error, 0.046; P = 0.029). The association was maintained after additional control for cardiovascular risk factors (β = -0.11; P = 0.031). The difference between cortisol responders and nonresponders was equivalent to approximately 2 years in aging. Conclusions: These findings suggest that cortisol responsivity may mediate, in part, the relationship between psychological stress and cellular aging.
MeSH term(s)	Aged ; Aging/genetics ; Aging/psychology ; Female ; Follow-Up Studies ; Humans ; Hydrocortisone/metabolism ; Leukocytes/metabolism ; Longitudinal Studies ; Male ; Middle Aged ; Saliva/chemistry ; Smoking ; Social Class ; Stress, Psychological/genetics ; Stress, Psychological/metabolism ; Stress, Psychological/psychology ; Telomere/metabolism ; Telomere Shortening
Chemical Substances	Hydrocortisone (WI4X0X7BPJ)
Language	English
Publishing date	2017-01-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/jc.2016-3035
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Article ; Online: Mechanisms of endothelial senescence.

Erusalimsky, Jorge D / Skene, Chris

Experimental physiology

2009 Volume 94, Issue 3, Page(s) 299–304

Abstract: When endothelial cells from different vascular beds are grown in culture they show a limited capacity to divide, eventually entering into a permanent and phenotypically distinctive non-dividing state referred to as 'replicative senescence'. Replicative ... ...

Abstract	When endothelial cells from different vascular beds are grown in culture they show a limited capacity to divide, eventually entering into a permanent and phenotypically distinctive non-dividing state referred to as 'replicative senescence'. Replicative senescence is thought to result from progressive shortening of telomeric DNA and consequent telomere dysfunction. More recently, it has been realised that senescence can also be induced by a variety of insults, including those causing intracellular oxidative stress. In this report, we review evidence for the occurrence of endothelial cell senescence in vivo. We will also examine the causes, mechanisms and regulation of this process as they emerge from our studies in cell culture, focusing in particular on the roles of oxidative stress, telomerase, growth factors and nitric oxide.
MeSH term(s)	Cell Division/physiology ; Cells, Cultured ; Cellular Senescence/physiology ; Endothelium, Vascular/cytology ; Endothelium, Vascular/physiology ; Humans ; Nitric Oxide/physiology ; Oxidative Stress/physiology ; Telomerase/physiology ; Telomere/physiology
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Telomerase (EC 2.7.7.49)
Language	English
Publishing date	2009-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1016295-1
ISSN	1469-445X ; 0958-0670
ISSN (online)	1469-445X
ISSN	0958-0670
DOI	10.1113/expphysiol.2008.043133
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