Advanced Glycation End Products and Their Involvement in Cardiovascular Disease

Yubero‐Serrano, Elena M.; Pérez-Martínez, Pablo

doi:10.1177/0003319720916301

Cited by 12 publications

(5 citation statements)

References 32 publications

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“…Similar to SAF studies, higher odds of poor muscle-related outcomes with higher levels of circulating AGEs were independent of cardiometabolic and renal diseases or related biomarkers, including CVD (Sun et al, 2012;Whitson et al, 2014), CVD medication (Ebert et al, 2019), diabetes mellitus (Dalal et al, 2009;Ebert et al, 2019;Sun et al, 2012), fasting glucose (Kim et al, 2018), HbA1c (Moriwaki et al, 2021), and serum creatinine (Ebert et al, 2019;Yang et al, 2019). These conditions have been associated with higher levels of circulating AGEs in the literature (Heidari et al, 2020;Kizer et al, 2014;Yubero-Serrano, Pérez-Martínez, 2020). The findings about the role of RAGEs in muscle mass and physical functioning were inconclusive (Dalal et al, 2009;Ebert et al, 2019;Kim et al, 2018;Moriwaki et al, 2021).…”

Section: Circulating Ages and Musclementioning

confidence: 65%

“…Residual confounding and shared biological pathways between ageing, common age-related diseases and sarcopenia may present additional challenges in discerning the strength and direction of AGEsmuscle relationship. Although most studies in this review have adjusted for a range of ageing diseases and factors linked to higher levels of AGEs in the literature (e.g., cardiometabolic and renal factors and diseases (Heidari et al, 2020;Kizer et al, 2014;Rajaobelina eta al, 2015;Viramontes Hörner, Taal, 2019;Yubero-Serrano, Pérez-Martínez, 2020), significant associations should be interpreted with caution. The presence of multiple diseases with overlapping pathophysiology in older adults makes it difficult to examine to what extent AGEs are byproducts of ageing and age-associated disease, including sarcopenia, and to what extent they actively contribute to disease development and progression (discussed in Chaudhuri eta l, 2018;Gugliucci, 2017;Ramasamy et al, 2005;Rowan et al, 2018;Semba et al, 2010b).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Advanced glycation end products in skeletal muscle health and sarcopenia: A systematic review of observational studies

Granic

Hurst

Dismore

et al. 2023

Mechanisms of Ageing and Development

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Section: Circulating Ages and Musclementioning

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Advanced glycation end products in skeletal muscle health and sarcopenia: A systematic review of observational studies

Granic

Hurst

Dismore

et al. 2023

Mechanisms of Ageing and Development

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“…Previous studies had shown that delayed wound healing in diabetes is not caused by local high-glucose concentration itself ( 56 ). Nevertheless, future studies will examine the presence of intermediate glycation products, and of advanced lipoxidation end-products in the donor tissues homogenates, given their atherogenic nature and their potential contribution to the pathologic vascular remodeling observed in the recipient rats ( 57 , 58 ).…”

Section: Discussionmentioning

confidence: 99%

Intralesional Infiltrations of Cell-Free Filtrates Derived from Human Diabetic Tissues Delay the Healing Process and Recreate Diabetes Histopathological Changes in Healthy Rats

Berlanga‐Acosta

Fernández‐Mayola

Mendoza‐Marí

et al. 2021

Front. Clin. Diabetes Healthc.

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Lower limb ulcers in type-2 diabetic patients are a frequent complication that tributes to amputation and reduces survival. We hypothesized that diabetic healing impairment and other histopathologic hallmarks are mediated by a T2DM-induced tissue priming/metabolic memory that can be transferred from humans to healthy recipient animals and consequently reproduce diabetic donor’s phenotypes. We examined the effect of human T2DM tissue homogenates injected into non-diabetic rat excisional wounds. Fresh granulation tissue, popliteal artery, and peroneal nerve of patients with T2DM were obtained following amputation. Post-mammoplasty granulation and post-traumatic amputation-tissue of normal subjects acted as controls. The homogenates were intralesionally injected for 6–7 days into rats’ excisional thickness wounds. Infiltration with the different homogenates caused impaired wound closure, inflammation, nerve degeneration, and arterial thickening (all P < 0.01 vs relevant control) resembling histopathology of diabetic donor tissues. Control materials caused marginal inflammation only. Infiltration with glycated bovine albumin provoked inflammation and wound healing delay but did not induce arterial thickening. The reproduction of human diabetic traits in healthy recipient animals through a tissue homogenate support the notion on the existence of tissue metabolic memory-associated and transmissible factors, involved in the pathogenesis of diabetic complications. These may have futuristic clinical implications for medical interventions.

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“…As diabetes mellitus (DM) is a major risk factor for atherosclerosis [ 50 ], advanced glycation end products (AGEs) increase arterial wall stiffness by cross-linking with elastin and collagen, or accelerate foam cell formation by cross-linking with oxLDL [ 51 ]. AGEs promote the transformation of macrophages into pro-inflammatory M1 subtype in plaques and reduce VSMCs contractile protein expression through the Notch pathway [ 52 ].…”

Section: Factors That Contribute To Vsmc Phenotypes Switchingmentioning

confidence: 99%

How vascular smooth muscle cell phenotype switching contributes to vascular disease

et al. 2022

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Vascular smooth muscle cells (VSMCs) are the most abundant cell in vessels. Earlier experiments have found that VSMCs possess high plasticity. Vascular injury stimulates VSMCs to switch into a dedifferentiated type, also known as synthetic VSMCs, with a high migration and proliferation capacity for repairing vascular injury. In recent years, largely owing to rapid technological advances in single-cell sequencing and cell-lineage tracing techniques, multiple VSMCs phenotypes have been uncovered in vascular aging, atherosclerosis (AS), aortic aneurysm (AA), etc. These VSMCs all down-regulate contractile proteins such as α-SMA and calponin1, and obtain specific markers and similar cellular functions of osteoblast, fibroblast, macrophage, and mesenchymal cells. This highly plastic phenotype transformation is regulated by a complex network consisting of circulating plasma substances, transcription factors, growth factors, inflammatory factors, non-coding RNAs, integrin family, and Notch pathway. This review focuses on phenotypic characteristics, molecular profile and the functional role of VSMCs phenotype landscape; the molecular mechanism regulating VSMCs phenotype switching; and the contribution of VSMCs phenotype switching to vascular aging, AS, and AA.

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Advanced Glycation End Products and Their Involvement in Cardiovascular Disease

Cited by 12 publications

References 32 publications

Advanced glycation end products in skeletal muscle health and sarcopenia: A systematic review of observational studies

Advanced glycation end products in skeletal muscle health and sarcopenia: A systematic review of observational studies

Intralesional Infiltrations of Cell-Free Filtrates Derived from Human Diabetic Tissues Delay the Healing Process and Recreate Diabetes Histopathological Changes in Healthy Rats

How vascular smooth muscle cell phenotype switching contributes to vascular disease

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