Low apoA-I is associated with insulin resistance in patients with impaired glucose tolerance: a cross-sectional study

Xu, Feng; Gao, Xia; Yao, Zhi; Xu, Yuan

doi:10.1186/s12944-017-0446-1

Cited by 28 publications

(26 citation statements)

References 51 publications

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“…This agent is a very important part of highdensity lipoprotein (HDL). ApoA-1 is an antioxidant and antiinflammatory agent, and it scavenges toxic phospholipids; stimulates reverse cholesterol transport, antithrombotic and profibrinolytic effects and attenuates endothelial dysfunction [8,16]. Therefore, carvedilol and apoA-1 have antiatherogenic effects that promote the functions of normal endothelium.…”

Section: Vascular Endotheliummentioning

confidence: 99%

“…Simvastatin and rosuvastatin also increase HDL levels. Therefore, HDL and apoA-1 levels can be increased by several methods [16]:…”

Section: Statinsmentioning

confidence: 99%

“…LDL, apoB and other toxic lipids from the lipid pool are removed by HDL and apoA-1, whose levels are increased by drug treatment as explained earlier. ApoA-1 also removes toxic phospholipids [16].…”

Section: Treatment Of Stable Atheromatous Plaquesmentioning

confidence: 99%

“…The proteases produced by macrophages remove smooth muscle cells and degrade collagen fibers. The extracellular matrix is damaged by MMP-9, which is an enzyme produced by macrophages [16]. As a result, the atheroma can rupture or ulcerate, and a thrombus may form on the ulcerated area.…”

Section: Treatment Of Stable Atheromatous Plaquesmentioning

confidence: 99%

“…Statins also inhibit MMP-9 secretion by macrophages and damaged endothelial cells. MMP-9 dissolves the extracellular matrix and increases the risk of plaque rupture, and amelioration of insulin resistance represses MMP-9 [16].…”

Section: Treatment Of Unstable or Vulnerable Atheromatous Plaques In mentioning

confidence: 99%

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A Cure for Coronary Artery Disease

Ahmad¹

2017

J Diabetes Metab

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To cure coronary artery disease, complete removal of atheroma from coronary arteries is necessary and may be achieved using pharmacological intervention. This hypothesis requires verification by a trial.The conditions that lead to the formation of atheroma are as follows:Insulin resistance and vascular endothelial dysfunction, Atherogenic dyslipidemia, Risk factors for coronary artery disease, Inflammation of coronary arteries, Drugs that increase insulin resistance.Atheroma formation begins with the formation of fatty streaks on the endothelium, which progress into stable or unstable atheromatous plaques. The unstable plaque has a thin fibrous cap that is prone to rupture. Unstable plaques contain a large lipid pool consisting of oxidized low-density lipoprotein (LDL), apoB and cholesterol that can grow; they are also have heavy inflammatory cell infiltration, including monocytes, macrophages and T cell lymphocytes. Moreover, debris from ruptured macrophages that were overloaded with lipids attracts more macrophages.The plaque can grow and protrude into the coronary artery lumen. Plaques exhibit overgrowth of vasa vasorum and they can rupture, leading to the formation of a large thrombus that may severely or completely obstruct the coronary artery. Hemorrhage may also occur in the plaque.Carvedilol and metformin promote plaque stability. The supply of lipids to the lipid pool in the plaque is reduced by statins and evolocumab, and lipids are removed from the lipid pool by apoA-1 and high-density lipoprotein (HDL) as their levels in the blood are increased. Severe inflammation is treated with carvedilol, metformin, statins and apoA.Growth of vasa vasorum is attributed to insulin resistance and can be reversed by carvedilol and metformin, thereby preventing hemorrhage. The size of the thrombus on a ruptured plaque can also be reduced by carvedilol, metformin and apoA-1, as these three agents prevent platelet aggregation. Thrombi are removed by endothelial thrombolysis. A thrombus may also form in the plaque from intraplaque hemorrhage; if present, the size of this type of thrombus will be small, as vasa vasorum are atrophic. In both cases, thrombi are removed by endothelial thrombolysis. Subsequently, healthy macrophages infiltrate and remove debris, after which the plaque changes to a fibrous nodule that can be removed by endothelial fibrinolysis. The plaque is then completely removed.

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Section: Vascular Endotheliummentioning

confidence: 99%

“…Simvastatin and rosuvastatin also increase HDL levels. Therefore, HDL and apoA-1 levels can be increased by several methods [16]:…”

Section: Statinsmentioning

confidence: 99%

Section: Treatment Of Stable Atheromatous Plaquesmentioning

confidence: 99%

Section: Treatment Of Stable Atheromatous Plaquesmentioning

confidence: 99%

Section: Treatment Of Unstable or Vulnerable Atheromatous Plaques In mentioning

confidence: 99%