Advanced Glycation End Products: Potential Mechanism and Therapeutic Target in Cardiovascular Complications under Diabetes

Yang, Ping; Feng, Jian; Peng, Qing; Liu, Xing; Fan, Zhongcai

doi:10.1155/2019/9570616

Cited by 108 publications

(88 citation statements)

References 139 publications

(141 reference statements)

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“…Since they are highly reactive and potent, glycating agents can generate more AGEs by reacting with proteins, in turn [98]. It was shown that AGE accumulation causes inflammation and destroys the normal structure and function of blood vessels, leading to vascular complications [101]. AGEs can also act by bonding to RAGEs (receptor for advanced glycation end-products) in plasma membrane and this interaction triggers different signaling pathways involved in apoptosis, inflammation, angiogenesis, and vasopermeability [102].…”

Section: Vitamin B6 and Diabetes Complicationsmentioning

confidence: 99%

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Vitamin B6 and Diabetes: Relationship and Molecular Mechanisms

Mascolo

Vernı̀

2020

IJMS

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Vitamin B6 is a cofactor for approximately 150 reactions that regulate the metabolism of glucose, lipids, amino acids, DNA, and neurotransmitters. In addition, it plays the role of antioxidant by counteracting the formation of reactive oxygen species (ROS) and advanced glycation end-products (AGEs). Epidemiological and experimental studies indicated an evident inverse association between vitamin B6 levels and diabetes, as well as a clear protective effect of vitamin B6 on diabetic complications. Interestingly, by exploring the mechanisms that govern the relationship between this vitamin and diabetes, vitamin B6 can be considered both a cause and effect of diabetes. This review aims to report the main evidence concerning the role of vitamin B6 in diabetes and to examine the underlying molecular and cellular mechanisms. In addition, the relationship between vitamin B6, genome integrity, and diabetes is examined. The protective role of this vitamin against diabetes and cancer is discussed.

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Section: Vitamin B6 and Diabetes Complicationsmentioning

confidence: 99%

“…Furthermore, AGEs increase the production of reactive oxygen species (ROS), which impact genome integrity [103,104]. The increase in ROS production can, in turn, promote the production of more AGEs, thereby forming a vicious circle [101].…”

Section: Vitamin B6 and Diabetes Complicationsmentioning

confidence: 99%

Vitamin B6 and Diabetes: Relationship and Molecular Mechanisms

Mascolo

Vernı̀

2020

IJMS

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“…Hyperglycemia induces the production of reactive oxygen species (ROS) and AGE [19]. These products can cause oxidative stress leading to abnormal bone homeostasis [20]. Osteoblast, the bone-forming cells were inhibited and osteoclast stimulated by AGEs, causing increased bone turnover [21].…”

Section: Review Osteoporotic Fractures and Diabetesmentioning

confidence: 99%

“…As a regulator of metabolic activity, many researchers started to appreciate the role of AMPK and tried to target this pathway as a treatment of many metabolic diseases such as DM and OS. Many substances have been shown to have activity on AMPK [16,20,38,42]. Among them, MF, which is already being used as a first-line medication for DM, shows a positive regulation effect of AMPK [37,[42][43].…”

Section: Ampk=amp Activated Protein Kinase; Amp=adenosine Monophosphatementioning

confidence: 99%

The Future of Metformin in the Prevention of Diabetes-Related Osteoporosis

Aung¹,

Amin²,

Gulraiz³

et al. 2020

Cureus

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As a worldwide aging population is on the rise, osteoporosis (OS) is becoming a global health burden. Therefore, many researchers and health authorities are looking into the potential prevention and treatment of OS. Although previously regarded as two separate pathological processes, diabetes (DM) and OS are now regarded as two conditions that can occur together. It is now believed that OS can develop as a complication of DM. This relationship is further evidenced through a reduction in bone mineral density in type-1 diabetes with a resulting increased risk of fracture. Although bone mineral density in type-2 diabetes mellitus is normal or increased, there is also increased fragility due to decreased bone quality. These abnormal bone qualities tend to occur through the production of reduced bone microvasculature and advanced glycation end product, AGE. Interestingly, one of the most common treatments for DM, metformin (MF), shows a promising result on the protection of diabetes and non-diabetes related bone turnover. It is believed that MF modulates its effect through the adenosine monophosphate-activated protein kinase (AMPK) pathway. Recent data regarded AMPK as a vital mediator of homeostasis. It is involved not only in glucose metabolism but also in osteogenesis. AMPK can directly influence the production of mature and good quality bone by decreasing osteoclasts, increasing osteoblast formation, and enhancing bone mineral deposition. As an activator of AMPK, MF also upregulates osteogenesis. Furthermore, MF can influence osteogenesis through a non-AMPK pathway, such as the fructose 1-6 phosphatase pathway, by reducing glucose levels. While already recognized as a safe and effective treatment for DM, this article discusses whether MF can be used for the prevention and treatment of OS.

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“…В развитии ХСН при СД2 ключевую стимулирующую роль отводят присущим диабету изменениям, включая инсулинорезистентность, гиперинсулинемию, гипергликемию и накопление конечных продуктов гликозилирования (КПГ) -advanced glycation end-products -AGEs [2,11]. Воздействие этих факторов определяет формирование трех основных патофизиологических механизмов:…”

Section: патофизиологические аспекты развития хсн у больных с сд2unclassified