Advanced glycation end products (AGEs) are generated by nonenzymatic modifications of macromolecules (proteins, lipids, and nucleic acids) by saccharides (glucose, fructose, and pentose) via Maillard reaction. The formed AGE molecules can be catabolized and cleared by glyoxalase I and II in renal proximal tubular cells. AGE-related diseases include physiological aging, neurodegenerative/neuroinflammatory diseases, diabetes mellitus (DM) and its complications, autoimmune/rheumatic inflammatory diseases, bone-degenerative diseases, and chronic renal diseases. AGEs, by binding to receptors for AGE (RAGEs), alter innate and adaptive immune responses to induce inflammation and immunosuppression via the generation of proinflammatory cytokines, reactive oxygen species (ROS), and reactive nitrogen intermediates (RNI). These pathological molecules cause vascular endothelial/smooth muscular/connective tissue-cell and renal mesangial/endothelial/podocytic-cell damage in AGE-related diseases. In the present review, we first focus on the cellular and molecular bases of AGE–RAGE axis signaling pathways in AGE-related diseases. Then, we discuss in detail the modes of action of newly discovered novel biomolecules and phytochemical compounds, such as Maillard reaction and AGE–RAGE signaling inhibitors. These molecules are expected to become the new therapeutic strategies for patients with AGE-related diseases in addition to the traditional hypoglycemic and anti-hypertensive agents. We particularly emphasize the importance of “metabolic memory”, the “French paradox”, and the pharmacokinetics and therapeutic dosing of the effective natural compounds associated with pharmacogenetics in the treatment of AGE-related diseases. Lastly, we propose prospective investigations for solving the enigmas in AGE-mediated pathological effects.

The Development of Maillard Reaction, and Advanced Glycation End Product (AGE)-Receptor for AGE (RAGE) Signaling Inhibitors as Novel Therapeutic Strategies for Patients with AGE-Related Diseases

Vascular diseases (VDs) including pulmonary arterial hypertension (PAH), atherosclerosis (AS) and coronary arterial diseases (CADs) contribute to the higher morbidity and mortality worldwide. Apolipoprotein A-I (Apo A-I) binding protein (AIBP) and Apo-AI negatively correlate with VDs. However, the mechanism by which AIBP and apo-AI regulate VDs still remains unexplained. Here, we provide an overview of the role of AIBP and apo-AI regulation of vascular diseases molecular mechanisms such as vascular energy homeostasis imbalance, oxidative and endoplasmic reticulum stress and inflammation in VDs. In addition, the role of AIBP and apo-AI in endothelial cells (ECs), vascular smooth muscle (VSMCs) and immune cells activation in the pathogenesis of VDs are explained. The in-depth understanding of AIBP and apo-AI function in the vascular system may lead to the discovery of VDs therapy.

Apolipoprotein-AI and AIBP synergetic anti-inflammation as vascular diseases therapy: the new perspective

Introduction: Antioxidant and hypoglycemic properties of some plant seeds are considered natural preventives for diabetic-associated glycation. This study is concerned with the evaluation of the bioactive components of black chia and garden cress seeds and the examination of their modulatory effects on hyperglycemia and associated glycation induced by streptozotocin (STZ) injection. Methods: Forty male rats were divided into 4 groups, 10 rats each: Group 1 (healthy control group); group 2 (diabetic group): rats injected STZ intraperitoneally to induce hyperglycemia; group 3 and group 4: rats treated (after diabetic induction) with 1 mL (20% w/w) black chia and garden cress seed extract, respectively. Results: STZ injection caused marked hyperglycemia, oxidative stress, glycation, and inflammation condition with disturbance in organs functions and structural alterations in pancreatic tissue, while; treatment with black chia and garden cress seed extracts showed remarkable (P < 0.05) modulatory effects on hyperglycemia and associated disorders. Conclusion: Black chia and garden cress seeds might be used in the management of diabetes and associated glycation.

The modulatory effects of black chia (Salvia hispanica) and garden cress (Lepidium sativum) seeds on Nε-CML formation in streptozotocin-injected rats

Objective The current research was designed to explore the relationship between the lipid accumulation index (LAP), coronary artery disease (CAD), and the triglyceride-glucose (TyG) index in patient with H-type hypertension. Methods From June 2021 to January 2022, our hospital’s information management system collected data on 186 patients with essential hypertension. The participants were categorized into two groups (H-type hypertension (n = 113) and non-H-type hypertension (n = 73)) based on their homocysteine levels. Both groups’ general condition, lipid accumulation index, triglyceride-glucose index, and Gensini score were compared to determine the factors influencing the severity of CAD in H-type hypertension patients. Results There were statistically significant differences (P < 0.05) in homocysteine (Hcy, GLP-1 and SAA) level, LAP, and TyG indexes, but not in body mass index (BMI), smoking, sex, age, total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), fasting plasma glucose (FPG), diastolic blood pressure, and systolic blood pressure. Additionally, there were substantial variations between the two groups regarding the number of lesion branches, degree of stenosis, and Gensini score (P > 0.05). patient with grade III to IV lesions had substantially higher LAP and TyG indices than those with stage I to II (P < 0.05). TyG (OR = 2.687) and TyG-LAP (OR = 4.512) were the factors determining the incidence of coronary artery disease in H-type hypertension, according to multivariate logistic regression analysis. The lesion number, stenosis degree, and Gensini score (P < 0.05) varied among both groups. LAP and TyG indexes were substantially greater in patients with double and triple vessel lesions than in those without lesions or with single vessel lesions (P < 0.05); similarly, these two indexes were considerably higher in individuals with grade III to IV lesions than in patients with grade I to II lesions (P < 0.05). As per the Pearson correlation analysis, the LAP, TyG indices and SAAlevel were adversely connected to the Gensini score (r = 0.254, 0.262, 0.299, P < 0.05), the GLP-1 level was negatively correlated to the Gensini score (r = −0.291, P < 0.05). TyG (OR = 2.687) and TyG-LAP (OR = 4.512) were the factors determining the frequency of coronary artery disease in H-type hypertension, according to multivariate logistic regression analysis. Conclusion In conclusion, the LAP and TyG indexes were observed to be closely related to the degree of CAD in H-type individuals with hypertension, which can better understand the pathogenesis of coronary artery disease in patients with H-type hypertension and is of great significance for guiding clinical doctors to carry out personalized treatment and management.

Correlation analysis of lipid accumulation index, triglyceride-glucose index and H-type hypertension and coronary artery disease

SIRT3-and FAK-mediated acetylation-phosphorylation crosstalk of NFATc1 regulates Nε-carboxymethyl-lysine-induced vascular calcification in diabetes mellitus.

Nϵ-carboxymethyl-lysine (CML), an advanced glycation end product, is involved in vascular calcification (VC) in diabetic atherosclerosis. This study aimed to investigate the effects of CML on VC in diabetic atherosclerosis induced by vascular smooth muscle cell (VSMC)-derived foam cells. Human studies, animal studies and cell studies were performed. The human study results from 100 patients revealed a poor blood glucose and lipid status and more severe coronary lesions and stenosis in patients with coronary artery disease and diabetes mellitus. Intraperitoneal injection of streptozotocin combined with a high-fat diet was used to build a diabetic atherosclerosis model in ApoE-/- mice. The animal study results indicated that CML accelerated VC progression in diabetic atherosclerosis by accelerating the accumulation of VSMC-derived foam cells in ApoE-/- mice. The cell study results illustrated that CML induced VSMC-derived foam cells apoptosis and aggravated foam cells calcification. Consistent with this finding, calcium content and the expression levels of alkaline phosphatase, bone morphogenetic protein 2 and runt-related transcription factor 2 were significantly elevated in A7r5 cells treated with oxidation-low-density lipoprotein and CML. Thus, we concluded that CML promoted VSMC-derived foam cells calcification to aggravate VC in diabetic atherosclerosis, providing evidence for the contribution of foam cells to diabetic VC.

Nϵ-Carboxymethyl-Lysine Deteriorates Vascular Calcification in Diabetic Atherosclerosis Induced by Vascular Smooth Muscle Cell-Derived Foam Cells.

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Nϵ-Carboxymethyl-Lysine Deteriorates Vascular Calcification in Diabetic Atherosclerosis Induced by Vascular Smooth Muscle Cell-Derived Foam Cells.