Journal of Cholesterol and Heart Disease

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Perspective - Journal of Cholesterol and Heart Disease (2022) Volume 6, Issue 6

Roles and therapeutic techniques in atherosclerosis.

Lemin Zhu*

Department of Cardiology, Hospital of Fujian Medical University, Quanzhou, Fujian Province, China

*Corresponding Author:
Lemin Zhu
Department of Cardiology,
Hospital of Fujian Medical University, Quanzhou,
Fujian Province, China
E-mail: [email protected]

Received:08-Nov-2022, Manuscript No. AACHD-22-84127; Editor assigned: 10-Nov-2022, PreQC No. AACHD-22-84127(PQ); Reviewed:25-Nov-2022, QC No. AACHD-22-84127; Revised:29-Nov-2022, Manuscript No. AACHD-22-84127(R); Published:06-Dec-2022, DOI: 10.35841/aachd-6.6.127

Citation: Zhu L. Roles and therapeutic techniques in atherosclerosis. J Cholest Heart Dis 2022;6(6):127

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Abstract

Atherosclerosis is a long-term inflammatory condition that causes plaque to accumulate inside the arteries. These plaques are mostly made of lipids, which cause turbulent flow and an inflammatory response, leading to Atherosclerotic Cardiovascular Disease (ASCVD). This exercise covers the diagnosis, management, and involvement of the interprofessional team in the care of patients with atherosclerosis. The primary global cause of morbidity and mortality is atherosclerosis. With an emphasis on recent discoveries about atherosclerosis indicators and risk factors, our goal was to evaluate the mechanism of atherosclerosis and associated risk factors.

Keywords

Atherosclerosis, Chronic inflammatory, Pathogenesis.

Introduction

About 50% of fatalities in developed countries are due to atherosclerosis, a chronic inflammatory disease of the arteries. It is thought to be the primary cause of ASCVD, which causes heart attacks, strokes, and peripheral arterial disease. It is primarily a lipid-driven process that is triggered by the accumulation of low-density lipoprotein and remnant lipoprotein particles and an active inflammatory process in focal areas of arteries, particularly at regions of disturbed non-laminar flow at branch points in the arteries [1].

Major improvements in our knowledge of the molecular and cellular connections in atherosclerosis have recently been made. These include cellular heterogeneity in atherosclerotic lesions that was previously unknown and was discovered using single-cell RNA sequencing (scRNA-seq). Additionally, it has been acknowledged that aging-related processes such clonal hematopoiesis and senescence probably plays a significant impact. Additionally, there is growing evidence linking the gut microbiota to atherosclerosis. The systems knowledge of the interaction of genetic and environmental risk factors for atherosclerosis and its link to cardio metabolic characteristics is still making significant progress. Finally, there have been fascinating developments in the field of diagnosis and treatment [2].

Low-density lipoprotein, a molecule that transports cholesterol through the blood, is presumably necessary for the development of atherosclerotic lesions. Hypertension, smoking, and diabetes mellitus are additional risk factors for atherosclerosis and the thrombotic problems that might result from it. Inflammation and clonal hematopoiesis are two newly emerging risk factors, and mounting evidence supports the immune system's involvement. Numerous insights into the processes connecting all of these risk factors to the formation of atheroma and the clinical symptoms of this illness have come from research on the cell and molecular biology of atherogenesis [3].

Assessment of cardiovascular disease risk and therapy targeting are made possible by a variety of diagnostic procedures, both invasive (such as selective coronary arteriography) and non-invasive (such as blood biomarkers, stress testing, CT, and nuclear scanning). There is a growing arsenal of therapeutics that can alter risk factors and have positive clinical effects; nevertheless, we still have a lot of work to do to ensure that everyone has access to these treatments and to increase adherence. However, the practical implementation of the research's results has advanced preventative measures, improved patients' clinical outcomes, and raised their quality of life. Continuous research and rapidly expanding understanding are expected to advance efforts to tackle this widespread chronic illness [4].

Atheromatous plaques, which are fatty deposits, develop in the inner layers of arteries as a result of the prevalent illness atherosclerosis. Small cholesterol crystals that are deposited in the intima and its supporting smooth muscle are the first step in the formation of these plaques. Once inside the arteries, the plaques expand due to the growth of adjacent smooth muscle and fibrous tissues, decreasing blood flow. Sclerosis or hardening of the arteries is brought on by fibroblasts producing connective tissue and calcium being deposited in the lesion. Finally, thrombosis and clot formation due to the uneven surface of the arteries cause an abrupt restriction of blood flow [5].

Conclusion

Atherosclerosis develops from the production of fatty streaks into atheroma and atherosclerotic plaque. Along with fibrinogen, it is one of the most significant pathogenic elements in atherogenic processes. Nitric oxide is a vasodilator and endothelial survival factor that promotes the proliferation and migration of endothelial cells. Peroxynitrate concentration raises in specific pathologic circumstances such severe hypercholesterolemia, which causes significant atherosclerotic damage. Utilizing antioxidants, especially herbal varieties, might be advantageous given the significance of oxidative stress and lipid oxidation in the development and progression of atherosclerosis and endothelial damage.

References

  1. Baradaran A. Lipoprotein (a), type 2 diabetes and nephropathy; the mystery continues. J Nephropathol. 2012;1(3):126.
  2.  Indexed at, Google Scholar, Cross Ref

  3. Freedman BI, Bostrom M, Daeihagh P, et al. Genetic factors in diabetic nephropathy. Clin J Am Soc Nephrol. 2007;2(6):1306-16.
  4. Indexed at, Google Scholar, Cross Ref

  5. Tavafi M. Complexity of diabetic nephropathy pathogenesis and design of investigations. J renal inj 2013;2(2):59.
  6. Indexed at, Google Scholar, Cross Ref

  7. Behradmanesh S, Nasri P. Serum cholesterol and LDL-C in association with level of diastolic blood pressure in type 2 diabetic patients. J renal inj. 2012;1(1):23.
  8. Indexed at, Google Scholar, Cross Ref

  9. Rudd JH, Hyafil F, Fayad ZA. Inflammation imaging in atherosclerosis. Arterioscler Thromb Vasc Biol. 2009;29(7):1009-16.
  10. Indexed at, Google Scholar, Cross Ref

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