Natural products: The role and mechanism in low‐density lipoprotein oxidation and atherosclerosis

Zhang, Shengyu; Li, Lingli; Chen, Wenxu; Xu, Suowen; Feng, Xiaohai; Zhang, Lei

doi:10.1002/ptr.7002

Cited by 55 publications

(40 citation statements)

References 175 publications

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“…It has been well established that NADPH-oxidase derived ROS from macrophages enhances the oxidation of LDL in the arterial wall, thereby promoting the formation of macrophage foam cells ( 75 , 76 ). Antioxidant treatment is considered a promising therapy for the prevention of AS, but currently available antioxidants show quite limited clinical utility ( 8 ). This may be due to the various ways of inducing and inhibiting oxidation in the body and the single role of antioxidants, which did not achieve the expected effect ( 8 , 77 ).…”

Section: Metformin In Regulating Macrophage Dysfunctionmentioning

confidence: 99%

“…Antioxidant treatment is considered a promising therapy for the prevention of AS, but currently available antioxidants show quite limited clinical utility ( 8 ). This may be due to the various ways of inducing and inhibiting oxidation in the body and the single role of antioxidants, which did not achieve the expected effect ( 8 , 77 ). Broad-spectrum ROS scavenging nanoparticles have a significant anti-atherosclerotic effect by decreasing local and systemic oxidative stress and inflammation ( 77 ).…”

Section: Metformin In Regulating Macrophage Dysfunctionmentioning

confidence: 99%

“…Lowering LDL plasma levels is a first line clinical treatment to decrease the risk profile of patients for cardiovascular and cerebrovascular diseases (7,9). In the initial stage of the development of atherosclerotic lesions, plasma lipoproteins trapped by modified proteoglycans accumulate in the subendothelial space, which can cause endothelial cell (EC) and platelet activation (8)(9)(10)(11)(12). Circulating monocytes adhere to the activated endothelium, penetrate the endothelium and differentiate into pro-inflammatory macrophages, which form foam cells by increasing the uptake of oxLDL.…”

Section: Introductionmentioning

confidence: 99%

“…The oxidation of low-density lipoprotein cholesterol (LDL-c) is considered to be one of the most important of the plethora of factors associated with the occurrence and development of AS ( 7 , 8 ). Lowering LDL plasma levels is a first line clinical treatment to decrease the risk profile of patients for cardiovascular and cerebrovascular diseases ( 7 , 9 ).…”

Section: Introductionmentioning

confidence: 99%

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Metformin, Macrophage Dysfunction and Atherosclerosis

Feng

Chen

et al. 2021

Front. Immunol.

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Metformin is one of the most widely prescribed hypoglycemic drugs and has the potential to treat many diseases. More and more evidence shows that metformin can regulate the function of macrophages in atherosclerosis, including reducing the differentiation of monocytes and inhibiting the inflammation, oxidative stress, polarization, foam cell formation and apoptosis of macrophages. The mechanisms by which metformin regulates the function of macrophages include AMPK, AMPK independent targets, NF-κB, ABCG5/8, Sirt1, FOXO1/FABP4 and HMGB1. On the basis of summarizing these studies, we further discussed the future research directions of metformin: single-cell RNA sequencing, neutrophil extracellular traps (NETs), epigenetic modification, and metformin-based combination drugs. In short, macrophages play an important role in a variety of diseases, and improving macrophage dysfunction may be an important mechanism for metformin to expand its pleiotropic pharmacological profile. In addition, the combination of metformin with other drugs that improve the function of macrophages (such as SGLT2 inhibitors, statins and IL-1β inhibitors/monoclonal antibodies) may further enhance the pleiotropic therapeutic potential of metformin in conditions such as atherosclerosis, obesity, cancer, dementia and aging.

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Section: Metformin In Regulating Macrophage Dysfunctionmentioning

confidence: 99%

Section: Metformin In Regulating Macrophage Dysfunctionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Metformin, Macrophage Dysfunction and Atherosclerosis

Feng

Chen

et al. 2021

Front. Immunol.

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“…LDL oxidation in vivo is likely to be influenced by local physiochemical and environmental factors like pH and availability of oxidants in order to oxidize LDL and its subpopulations. Factors like antioxidant content, particle size and fatty acid (FA) composition are also important determinant of LDL oxidation [39][40][41][42].…”

Section: Oxidative Modification Of Ldlmentioning

confidence: 99%

Oxidative Modification of Lipoproteins: A Potential Role of Oxidized Small dense LDL in Enhanced Atherogenicity

Alsaweed

2021

JPRI

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Atherosclerosis (AS) is a multifaceted inflammatory syndrome of the arterial wall to which number of mediators have been implicated in lesion progression. Triglyceride (TG)-rich lipoproteins consist of the large diversity of lipoprotein particles that fluctuate in density, size, and apolipoprotein composition. Two foremost phenotypes, on basis of size, chemical configuration, and density, of low-density-lipoprotein (LDL) have been recognized i.e., pattern A, having LDL diameter greater than 25.5nm (large buoyant LDL or lb-LDL) and pattern B, having LDL diameter less than or equal to 25.5nm (small-dense LDL or sd-LDL). Small-dense low-density-lipoprotein (sd-LDL) particles are produced by potential intravascular hydrolysis of TG-rich VLDL particles via lipoprotein lipases (LPLs), hepatic lipases (HLs) and cholesterol ester transfer protein (CETP). sd-LDL is more atherogenic due to its smaller size, increased penetration into the arterial wall, extended plasma half-life, lesser binding affinity for LDL receptors (LDL-R) as well as lower resistance to oxidative stress when equated with lb-LDL. The higher atherogenic potential of sd-LDL is due to its enhanced susceptibility to oxidation, owing to high polyunsaturated fatty acids (PUFA), low cholesterol and Apoprotein B (ApoB) content. An enhanced understanding of sd-LDL metabolism at the molecular level, transport and clearance may result in the development of sd-LDL as an independent predictive marker for AS events and may be used to maintain cholesterol homeostasis and prevent the succession of AS.

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Methyl benzoate derivatives: in vitro Paraoxonase 1 inhibition and in silico studies

Korkmaz

Türkeş

Demir

et al. 2022

J Biochem & Molecular Tox

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Paraoxonase 1 (PON1) can metabolize some compounds such as aromatic carboxylic acid and unsaturated aliphatic esters, arylesters, cyclic carbonate, plucuronide drugs, some carbamate insecticide classes, nerve gases, and lactone compounds. Methyl benzoate has recently been shown to display potent toxicity against several insect species. In the current study, we aimed to investigate the effect of the methyl benzoate compounds (1–17) on PON1 activity. Methyl benzoate compounds inhibited PON1 with KI values ranging from 25.10 ± 4.73 to 502.10 ± 64.72 μM. Compound 10 (methyl 4‐amino‐2‐bromo benzoate) showed the best inhibition (KI = 25.10 ± 4.73 μM). Furthermore, using the ADME‐Tox, Glide XP, and MM‐GBSA tools of the Schrödinger Suite 2021‐4, a complete ligand–receptor interaction prediction was performed to characterize the methyl benzoates (1–17), probable binding modalities versus the PON1.

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Natural products: The role and mechanism in low‐density lipoprotein oxidation and atherosclerosis

Cited by 55 publications

References 175 publications

Metformin, Macrophage Dysfunction and Atherosclerosis

Metformin, Macrophage Dysfunction and Atherosclerosis

Oxidative Modification of Lipoproteins: A Potential Role of Oxidized Small dense LDL in Enhanced Atherogenicity

Methyl benzoate derivatives: in vitro Paraoxonase 1 inhibition and in silico studies

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