A potential strategy for treating atherosclerosis: improving endothelial function via AMP-activated protein kinase

Gao, Feng; Chen, Jiemei; Zhu, Haibo

doi:10.1007/s11427-017-9285-1

Cited by 45 publications

(26 citation statements)

References 49 publications

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“…In addition to NO deficiency and intestinal flora, other factors including oxidative stress (Nakahira et al, 2011), endoplasmic reticulum stress (Battson et al, 2017;Luchetti et al, 2017), mitochondrial dysfunction (Gao et al, 2018), hypoxia (Feng et al, 2017a), homocysteine (Esse and Barroso, 2019), and immune activation (Pan et al, 2017) are also closely related with endothelial inflammation and dysfunction in cardiovascular diseases. With in-depth research, our knowledge on the underlying mechanisms of H 2 S-mediated suppression of endothelial cell inflammation is expanding and it is now apparent that interactions between H 2 S and endothelial inflammation-regulated pathways may be proposed as a promising approach for cardiovascular disease therapy.…”

Section: Concluding Remarks and Future Perspectivesmentioning

confidence: 99%

Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide

et al. 2020

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Endothelial cells are important constituents of blood vessels that play critical roles in cardiovascular homeostasis by regulating blood fluidity and fibrinolysis, vascular tone, angiogenesis, monocyte/leukocyte adhesion, and platelet aggregation. The normal vascular endothelium is taken as a gatekeeper of cardiovascular health, whereas abnormality of vascular endothelium is a major contributor to a plethora of cardiovascular ailments, such as atherosclerosis, aging, hypertension, obesity, and diabetes. Endothelial dysfunction is characterized by imbalanced vasodilation and vasoconstriction, elevated reactive oxygen species (ROS), and proinflammatory factors, as well as deficiency of nitric oxide (NO) bioavailability. The occurrence of endothelial dysfunction disrupts the endothelial barrier permeability that is a part of inflammatory response in the development of cardiovascular diseases. As such, abrogation of endothelial cell activation/inflammation is of clinical relevance. Recently, hydrogen sulfide (H 2 S), an entry as a gasotransmitter, exerts diverse biological effects through acting on various targeted signaling pathways. Within the cardiovascular system, the formation of H 2 S is detected in smooth muscle cells, vascular endothelial cells, and cardiomyocytes. Disrupted H 2 S bioavailability is postulated to be a new indicator for endothelial cell inflammation and its associated endothelial dysfunction. In this review, we will summarize recent advances about the roles of H 2 S in endothelial cell homeostasis, especially under pathological conditions, and discuss its putative therapeutic applications in endothelial inflammation-associated cardiovascular disorders.

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Section: Concluding Remarks and Future Perspectivesmentioning

confidence: 99%

Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide

et al. 2020

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“…Activation of AMPK inhibits the production of reactive oxygen species, ER stress, and Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and increase the bioavailability of nitric oxide. Consequently, it limits pro-inflammatory factors production induced by dyslipidemia and hyperglycemia [75]. Furthermore, AMPK may downregulate FFA-induced increases in NF-κB transactivation [76].…”

Section: Inflammationmentioning

confidence: 99%

Vasculoprotective Effects of Vildagliptin. Focus on Atherogenesis

Wiciński

Górski

Wódkiewicz

et al. 2020

IJMS

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Vildagliptin is a representative of Dipeptidyl Peptidase-4 (DPP-4) inhibitors, antihyperglycemic drugs, approved for use as monotherapy and combination therapy in type 2 diabetes mellitus. By inhibiting enzymatic decomposition, DPP-4 inhibitors increase the half-life of incretins such as GLP-1 (Glucagon-like peptide-1) and GIP (Gastric inhibitors polypeptide) and prolong their action. Some studies present results suggesting the anti-sclerotic and vasculoprotective effects of vildagliptin reaching beyond glycemic control. Vildagliptin is able to limit inflammation by suppression of the NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) signaling pathway and proinflammatory agents such as TNF-α (tumor necrosis factor α), IL-1β (Interleukin-1β), and IL-8 (Interleukin 8). Moreover, vildagliptin regulates lipid metabolism; attenuates postprandial hypertriglyceridemia; and lowers serum triglycerides, apolipoprotein B, and blood total cholesterol levels. This DPP-4 inhibitor also reduces macrophage foam cell formation, which plays a key role in atheromatous plaque formation and stability. Vildagliptin reduces vascular stiffness via elevation of nitric oxide synthesis, improves vascular relaxation, and results in reduction in both systolic and diastolic blood pressure. Treatment with vildagliptin lowers the level of PAI-1 presenting possible antithrombotic effect. By affecting the endothelium, inflammation, and lipid metabolism, vildagliptin may affect the development of atherosclerosis at its various stages. The article presents a summary of the studies assessing vasculoprotective effects of vildagliptin with special emphasis on atherogenesis.

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“…In many pathological conditions, the body adapts to these challenges by activating AMPK, which modulates numerous downstream targets [47]. The concept that the activation of AMPK is beneficial to various diseases has been widely recognized [56][57][58]. It has been proved that activating AMPK can improve cardiometabolic disease [7], protect from myocardial ischemia [7], inhibit cardiac hypertrophy and cardiomyopathy [8,[59][60][61], protect heart function and delay heart failure [7,[62][63][64][65], and antiarrhythmia [10].…”

mentioning

confidence: 99%

AMPK: a balancer of the renin–angiotensin system

Liu

et al. 2019

Bioscience Reports

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The renin–angiotensin system (RAS) is undisputedly well-studied as one of the oldest and most critical regulators for arterial blood pressure, fluid volume, as well as renal function. In recent studies, RAS has also been implicated in the development of obesity, diabetes, hyperlipidemia, and other diseases, and also involved in the regulation of several signaling pathways such as proliferation, apoptosis and autophagy, and insulin resistance. AMP-activated protein kinase (AMPK), an essential cellular energy sensor, has also been discovered to be involved in these diseases and cellular pathways. This would imply a connection between the RAS and AMPK. Therefore, this review serves to draw attention to the cross-talk between RAS and AMPK, then summering the most recent literature which highlights AMPK as a point of balance between physiological and pathological functions of the RAS.

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A potential strategy for treating atherosclerosis: improving endothelial function via AMP-activated protein kinase

Cited by 45 publications

References 49 publications

Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide

Role of Endothelial Dysfunction in Cardiovascular Diseases: The Link Between Inflammation and Hydrogen Sulfide

Vasculoprotective Effects of Vildagliptin. Focus on Atherogenesis

AMPK: a balancer of the renin–angiotensin system

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