Effects of advanced glycation end products (AGEs) on the differentiation potential of primary stem cells: a systematic review

Xu, Kuishuai; Zhang, Liang; Yu, Ning; Ren, Zhongkai; Wang, Tianrui; Zhang, Yingze; Zhao, Xia; Yu, Tengbo

doi:10.1186/s13287-023-03324-5

Cited by 7 publications

(5 citation statements)

References 139 publications

(166 reference statements)

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“…Advanced glycation end products (AGEs) are toxic compounds that are formed under hyperglycemic conditions and can lead to tissue damage and organ dysfunction [97]. The accumulation of AGEs can impair the healing process and cause serious damage to organs and tissues [98]. AGEs can also interact with RAGEs and activate NADPH, leading to the generation of excess ROS [99].…”

Section: Oxidative Stress Inhibition Promotes Cell Viability In Vitromentioning

confidence: 99%

Hypoxia-Inducible Factor and Oxidative Stress in Tendon Degeneration: A Molecular Perspective

Shahid,

Morya,

et al. 2024

Antioxidants

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Tendinopathy is a debilitating condition marked by degenerative changes in the tendons. Its complex pathophysiology involves intrinsic, extrinsic, and physiological factors. While its intrinsic and extrinsic factors have been extensively studied, the role of physiological factors, such as hypoxia and oxidative stress, remains largely unexplored. This review article delves into the contribution of hypoxia-associated genes and oxidative-stress-related factors to tendon degeneration, offering insights into potential therapeutic strategies. The unique aspect of this study lies in its pathway-based evidence, which sheds light on how these factors can be targeted to enhance overall tendon health.

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Section: Oxidative Stress Inhibition Promotes Cell Viability In Vitromentioning

confidence: 99%

Hypoxia-Inducible Factor and Oxidative Stress in Tendon Degeneration: A Molecular Perspective

Shahid,

Morya,

et al. 2024

Antioxidants

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“…Glycation, a non-enzymatic reaction where reducing sugars react with proteins, lipids, and nucleic acids, leads to the formation of AGEs. These AGEs accumulate in various tissues, including the brain and lungs, causing cellular dysfunction and disease progression ( Xu et al, 2023 ).…”

Section: Oxidative Stress In Brain–lung Crosstalkmentioning

confidence: 99%

Oxidative stress in the brain–lung crosstalk: cellular and molecular perspectives

Kong,

Fan,

Zhang

et al. 2024

Front. Aging Neurosci.

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Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to counteract their harmful effects, playing a key role in the pathogenesis of brain and lung-related diseases. This review comprehensively examines the intricate mechanisms by which oxidative stress influences cellular and molecular pathways, contributing to neurodegenerative, cardiovascular, and respiratory disorders. Emphasizing the detrimental effects on both brain and lung health, we discuss innovative diagnostic biomarkers, such as 8-hydroxy-2′-deoxyguanosine (8-OHdG), and the potential of antioxidant therapies. For these topics, we provide insights into future research directions in the field of oxidative stress treatment, including the development of personalized treatment approaches, the discovery and validation of novel biomarkers, and the development of new drug delivery systems. This review not only provides a new perspective on understanding the role of oxidative stress in brain and lung-related diseases but also offers new insights for future clinical treatments.

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“…Similarly, another Table 1. Examples of glycation's contribution to each hallmark of ageing (as defined by Lopez-Otìn et al [3,11,[15][16][17][18][19][20][21][22][23][24]). hallmark of ageing (as defined by [11]) examples of glycations' contribution genome instability…”

Section: (B) Correlations Between Glycation and Body Massmentioning

confidence: 99%

Glycation resistance and life-history traits: lessons from non-conventional animal models

Duval,

Criscuolo,

Bertile

2024

Biol. Lett.

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Glycation reactions play a key role in the senescence process and are involved in numerous age-related pathologies, such as diabetes complications or Alzheimer’s disease. As a result, past studies on glycation have mostly focused on human and laboratory animal models for medical purposes. Very little is known about glycation and its link to senescence in wild animal species. Yet, despite feeding on high-sugar diets, several bat and bird species are long-lived and seem to escape the toxic effects of high glycaemia. The study of these models could open new avenues both for understanding the mechanisms that coevolved with glycation resistance and for treating the damaging effects of glycations in humans. Our understanding of glycaemia’s correlation to proxies of animals’ pace of life is emerging in few wild species; however, virtually nothing is known about their resistance to glycation, nor on the relationship between glycation, species’ life-history traits and individual fitness. Our review summarizes the scarce current knowledge on the links between glycation and life-history traits in non-conventional animal models, highlighting the predominance of avian research. We also investigate some key molecular and physiological parameters involved in glycation regulation, which hold promise for future research on fitness and senescence of individuals.

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Effects of advanced glycation end products (AGEs) on the differentiation potential of primary stem cells: a systematic review

Cited by 7 publications

References 139 publications

Hypoxia-Inducible Factor and Oxidative Stress in Tendon Degeneration: A Molecular Perspective

Hypoxia-Inducible Factor and Oxidative Stress in Tendon Degeneration: A Molecular Perspective

Oxidative stress in the brain–lung crosstalk: cellular and molecular perspectives

Glycation resistance and life-history traits: lessons from non-conventional animal models

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