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      Functional roles and mechanisms of ginsenosides from Panax ginseng in atherosclerosis

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          Abstract

          Atherosclerosis (AS) is a leading cause of cardiovascular diseases (CVDs) and it results in a high rate of death worldwide, with an increased prevalence with age despite advances in lifestyle management and drug therapy. Atherosclerosis is a chronic progressive inflammatory process, and it mainly presents with lipid accumulation, foam cell proliferation, inflammatory response, atherosclerotic plaque formation and rupture, thrombosis, and vascular calcification. Therefore, there is a great need for reliable therapeutic drugs or remedies to cure or alleviate atherosclerosis and reduce the societal burden. Ginsenosides are natural steroid glycosides and triterpene saponins obtained mainly from the plant ginseng. Several recent studies have reported that ginsenosides have a variety of pharmacological activities against several diseases including inflammation, cancer and cardiovascular diseases. This review focuses on describing the different pharmacological functions and underlying mechanisms of various active ginsenosides (Rb1,-Rd, -F, -Rg1, -Rg2, and -Rg3, and compound K) for atherosclerosis, which could provide useful insights for developing novel and effective anti-cardiovascular drugs.

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          Origin and physiological roles of inflammation.

          Ruslan Medzhitov (2008)
          Inflammation underlies a wide variety of physiological and pathological processes. Although the pathological aspects of many types of inflammation are well appreciated, their physiological functions are mostly unknown. The classic instigators of inflammation - infection and tissue injury - are at one end of a large range of adverse conditions that induce inflammation, and they trigger the recruitment of leukocytes and plasma proteins to the affected tissue site. Tissue stress or malfunction similarly induces an adaptive response, which is referred to here as para-inflammation. This response relies mainly on tissue-resident macrophages and is intermediate between the basal homeostatic state and a classic inflammatory response. Para-inflammation is probably responsible for the chronic inflammatory conditions that are associated with modern human diseases.
          Article 0 comments Cited 1810 times – based on 0 reviews     Review now
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            Vascular Smooth Muscle Cells in Atherosclerosis.

            Martin Bennett, Sanjay Sinha, Gary Owens (2016)
            The historical view of vascular smooth muscle cells (VSMCs) in atherosclerosis is that aberrant proliferation of VSMCs promotes plaque formation, but that VSMCs in advanced plaques are entirely beneficial, for example preventing rupture of the fibrous cap. However, this view has been based on ideas that there is a homogenous population of VSMCs within the plaque, that can be identified separate from other plaque cells (particularly macrophages) using standard VSMC and macrophage immunohistochemical markers. More recent genetic lineage tracing studies have shown that VSMC phenotypic switching results in less-differentiated forms that lack VSMC markers including macrophage-like cells, and this switching directly promotes atherosclerosis. In addition, VSMC proliferation may be beneficial throughout atherogenesis, and not just in advanced lesions, whereas VSMC apoptosis, cell senescence, and VSMC-derived macrophage-like cells may promote inflammation. We review the effect of embryological origin on VSMC behavior in atherosclerosis, the role, regulation and consequences of phenotypic switching, the evidence for different origins of VSMCs, and the role of individual processes that VSMCs undergo in atherosclerosis in regard to plaque formation and the structure of advanced lesions. We think there is now compelling evidence that a full understanding of VSMC behavior in atherosclerosis is critical to identify therapeutic targets to both prevent and treat atherosclerosis.
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              Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness

              Andrew L. Durham, Mei Speer, Marta Scatena … (2018)
              Abstract Vascular calcification is associated with a significant increase in all-cause mortality and atherosclerotic plaque rupture. Calcification has been determined to be an active process driven in part by vascular smooth muscle cell (VSMC) transdifferentiation within the vascular wall. Historically, VSMC phenotype switching has been viewed as binary, with the cells able to adopt a physiological contractile phenotype or an alternate ‘synthetic’ phenotype in response to injury. More recent work, including lineage tracing has however revealed that VSMCs are able to adopt a number of phenotypes, including calcific (osteogenic, chondrocytic, and osteoclastic), adipogenic, and macrophagic phenotypes. Whilst the mechanisms that drive VSMC differentiation are still being elucidated it is becoming clear that medial calcification may differ in several ways from the intimal calcification seen in atherosclerotic lesions, including risk factors and specific drivers for VSMC phenotype changes and calcification. This article aims to compare and contrast the role of VSMCs in driving calcification in both atherosclerosis and in the vessel media focusing on the major drivers of calcification, including aging, uraemia, mechanical stress, oxidative stress, and inflammation. The review also discusses novel findings that have also brought attention to specific pro- and anti-calcifying proteins, extracellular vesicles, mitochondrial dysfunction, and a uraemic milieu as major determinants of vascular calcification.
              Article 0 comments Cited 327 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Jae Youl Cho
                Yanyan Yang
                Tao Yu
                Journal
                Journal ID (nlm-ta): J Ginseng Res
                Journal ID (iso-abbrev): J Ginseng Res
                Title: Journal of Ginseng Research
                Publisher: Elsevier
                ISSN (Print): 1226-8453
                ISSN (Electronic): 2093-4947
                Publication date PMC-release: 16 July 2020
                Publication date (Print): January 2021
                Publication date (Electronic): 16 July 2020
                Volume: 45
                Issue: 1
                Pages: 22-31
                Affiliations
                [a ]Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, China
                [b ]Department of Pharmacology, School of Pharmacy, Qingdao University, China
                [c ]Institute for translational medicine, School of Basic Medicine, Qingdao University, China
                [d ]School of Basic Medicine, Qingdao University, China
                [e ]Department of Integrative Biotechnology, Sungkyunkwan University, Suwon, Republic of Korea
                Author notes
                [∗ ]Corresponding author. Department of Cardiac Ultrasound, Affiliated Hospital of Qingdao University, Institute for Translational medicine, Qingdao University, 266000, China. yutao0112@ 123456qdu.edu.cn
                [∗∗ ]Corresponding author. Institute for Translational medicine, Qingdao University, China. yangyy1201@ 123456qdu.edu.cn
                [∗∗∗ ]Corresponding author. Department of Integrative Biotechnology, Sungkyunkwan University, 300 Chuncheon-Dong, Suwon, 16419, Republic of Korea. jaecho@ 123456skku.edu
                [#]

                These authors are equally to this work.

                Article
                Publisher Item ID: S1226-8453(20)30113-5
                DOI: 10.1016/j.jgr.2020.07.002
                PMC ID: 7790891
                PubMed ID: 33437153
                SO-VID: 39f23a92-525d-4222-9931-4dad0339cdbe
                Copyright © © 2020 The Korean Society of Ginseng. Publishing services by Elsevier B.V.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 24 February 2020
                Date revision received : 17 May 2020
                Date accepted : 7 July 2020
                Categories
                Subject: Review Article

                Keywords: atherosclerosis,ginsenosides,endothelial cell,inflammation,macrophage
                Data availability:
                Keywords: atherosclerosis, ginsenosides, endothelial cell, inflammation, macrophage

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