Commentary - Journal of Hypertension and Heart Care (2023) Volume 6, Issue 2

The role of cholesterol and inflammation in patients with atherosclerosis

Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical School, Ann Arbor, MI 48109, USA

*Corresponding Author:

Mbamalu ON
Department of Internal Medicine
Cardiovascular Center
University of Michigan Medical School
Ann Arbor, MI 48109, USA
E-mail: chen@umich.edu

Received: 24-Mar-2023, Manuscript No. AAJHHC-23-97213; Editor assigned: 25-Mar-2023, PreQC No. AAJHHC-23-97213(PQ); Reviewed: 08-Apr-2023, QC No. AAJHHC-23-97213; Revised: 10-Apr-2023, Manuscript No. AAJHHC-23-97213(R); Published: 18-Apr-2023, DOI: 10.35841/AAJHHC-6.2.144

Citation: Zhang C. The role of cholesterol and inflammation in patients with atherosclerosis. J Hypertens Heart Care. 2023;6(2):144

Introduction

Atherosclerosis is a chronic inflammatory disease that is characterized by the accumulation of lipids, particularly cholesterol, in the arterial wall. This accumulation results in the formation of atherosclerotic plaques that can lead to the development of cardiovascular disease (CVD), including coronary artery disease, stroke, and peripheral arterial disease. The pathophysiology of atherosclerosis is complex and involves numerous processes, including inflammation and the dysregulation of lipid metabolism. In this essay, we will discuss the role of cholesterol and inflammation in patients with atherosclerosis.

Cholesterol is an essential component of cell membranes, and it is also required for the synthesis of hormones and bile acids. Cholesterol is transported in the blood by lipoproteins, which are composed of lipids and proteins. Low-density lipoprotein (LDL) is commonly known as "bad" cholesterol, as it can deposit cholesterol in the arterial wall and promote atherosclerosis. High-density lipoprotein (HDL), on the other hand, is known as "good" cholesterol, as it helps remove excess cholesterol from the arterial wall and transport it back to the liver for excretion [1]. In patients with atherosclerosis, the balance between LDL and HDL cholesterol is disrupted, leading to the accumulation of cholesterol in the arterial wall. The presence of LDL cholesterol in the arterial wall initiates an inflammatory response, which is a key component of the development and progression of atherosclerosis. The inflammatory response is mediated by various cells, including macrophages, T cells, and endothelial cells.

Macrophages are immune cells that play a crucial role in the inflammatory response in atherosclerosis. Macrophages take up oxidized LDL cholesterol through scavenger receptors, leading to the formation of foam cells, which are a hallmark of atherosclerosis. Foam cells release pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), which contribute to the inflammatory response in the arterial wall [2].

T cells also play a critical role in the inflammatory response in atherosclerosis. T cells are activated in response to oxidized LDL cholesterol, and they release cytokines that promote inflammation and the recruitment of other immune cells to the arterial wall. T cells also contribute to the formation of atherosclerotic plaques by producing matrix metalloproteinases (MMPs), which can degrade the extracellular matrix and weaken the fibrous cap of the plaque, increasing the risk of rupture and thrombosis.

Endothelial cells line the inner surface of blood vessels and play a critical role in regulating vascular function. In patients with atherosclerosis, endothelial cells become activated and release pro-inflammatory cytokines, adhesion molecules, and chemokines, which promote the recruitment of immune cells to the arterial wall. Endothelial dysfunction, characterized by impaired nitric oxide bioavailability, is a hallmark of atherosclerosis and contributes to the development of hypertension and other cardiovascular risk factors.

Inflammation in atherosclerosis is also mediated by the activation of the nuclear factor-kappa B (NF-κB) signaling pathway [3]. NF-κB is a transcription factor that regulates the expression of genes involved in inflammation, cell proliferation, and apoptosis. In patients with atherosclerosis, NF-κB is activated in response to oxidative stress and the presence of inflammatory cytokines, leading to the upregulation of pro-inflammatory genes and the downregulation of anti-inflammatory genes.

In addition to the role of inflammation, dyslipidemia is a significant contributor to the development and progression of atherosclerosis. Dyslipidemia is characterized by high levels of LDL cholesterol and low levels of HDL cholesterol. Statins are a class of drugs that lower LDL cholesterol levels and have been shown to reduce the risk of cardiovascular events in patients with atherosclerosis. Statins work by inhibiting the enzyme HMG-CoA reductase, which is involved in the synthesis of cholesterol. By reducing LDL cholesterol levels, statins can decrease the accumulation of cholesterol in the arterial wall and reduce the inflammatory response.

Another class of drugs that can reduce the risk of cardiovascular events in patients with atherosclerosis are monoclonal antibodies that target proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 is a protein that regulates LDL receptor levels on the surface of hepatocytes, which are liver cells that are involved in cholesterol metabolism. By inhibiting PCSK9, these drugs can increase LDL receptor levels and decrease LDL cholesterol levels. In addition to pharmacological interventions, lifestyle modifications are also essential in the management of patients with atherosclerosis. Diet and exercise can help reduce LDL cholesterol levels and improve vascular function. A diet rich in fruits, vegetables, whole grains, and lean proteins, and low in saturated and trans fats, can help reduce LDL cholesterol levels. Regular exercise can improve endothelial function and reduce inflammation.

In conclusion, atherosclerosis is a chronic inflammatory disease that is characterized by the accumulation of cholesterol in the arterial wall. The dysregulation of lipid metabolism and the activation of the inflammatory response are key components of the pathophysiology of atherosclerosis [4,5]. The development and progression of atherosclerosis can be reduced through pharmacological interventions, such as statins and PCSK9 inhibitors, as well as lifestyle modifications, such as diet and exercise. Understanding the role of cholesterol and inflammation in atherosclerosis is essential for the prevention and management of cardiovascular disease.

References

1. Xu XH, Equils O. Toll-like receptor-4 is expressed by macrophages in murine and human lipid-rich atherosclerotic plaques and upregulated by oxidized LDL. Circulation. 2001; 104(25):3103-8.

Indexed at, Google Scholar, Cross Ref

2. Váradi J, Hermenean A. Pharmacokinetic properties of fluorescently labelled hydroxypropyl-beta-cyclodextrin. Biomolecules.2019;9(10):509.

Indexed at, Google Scholar, Cross Ref

3. He J, Yang Y. Shuttle/sink model composed of β-cyclodextrin and simvastatin-loaded discoidal reconstituted high-density lipoprotein for enhanced cholesterol efflux and drug uptake in macrophage/foam cells. J Mater ChemB. 2020;8 (7):1496-1506.

Indexed at, Google Scholar, Cross Ref

4. Viatour P, Chariot A.  Phosphorylation of NF-κB and IκB proteins: implications in cancer and inflammation Trends. Biochem Sci.2005; 30(1):43-52.

Indexed at, Google Scholar, Cross Ref

5. Guo Y, Zhang J. Perhexiline activates KLF14 and reduces atherosclerosis by modulating ApoA-I production. J Clin Invest. 2015;125(10):3819-30

Indexed at, Google Scholar, Cross Ref