26
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Signaling Pathways and Key Genes Involved in Regulation of foam Cell Formation in Atherosclerosis

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Atherosclerosis is associated with acute cardiovascular conditions, such as ischemic heart disease, myocardial infarction, and stroke, and is the leading cause of morbidity and mortality worldwide. Our understanding of atherosclerosis and the processes triggering its initiation is constantly improving, and, during the last few decades, many pathological processes related to this disease have been investigated in detail. For example, atherosclerosis has been considered to be a chronic inflammation triggered by the injury of the arterial wall. However, recent works showed that atherogenesis is a more complex process involving not only the immune system, but also resident cells of the vessel wall, genetic factors, altered hemodynamics, and changes in lipid metabolism. In this review, we focus on foam cells that are crucial for atherosclerosis lesion formation. It has been demonstrated that the formation of foam cells is induced by modified low-density lipoprotein (LDL). The beneficial effects of the majority of therapeutic strategies with generalized action, such as the use of anti-inflammatory drugs or antioxidants, were not confirmed by clinical studies. However, the experimental therapies targeting certain stages of atherosclerosis, among which are lipid accumulation, were shown to be more effective. This emphasizes the relevance of future detailed investigation of atherogenesis and the importance of new therapies development.

          Related collections

          Most cited references47

          • Record: found
          • Abstract: found
          • Article: not found

          Pathogenesis of atherosclerosis.

          Atherosclerosis is a multifocal, smoldering, immunoinflammatory disease of medium-sized and large arteries fuelled by lipids. Endothelial cells, leukocytes, and intimal smooth muscle cells are the major players in the development of this disease. The most devastating consequences of atherosclerosis, such as heart attack and stroke, are caused by superimposed thrombosis. Therefore, the vital question is not why atherosclerosis develops but rather why atherosclerosis, after years of indolent growth, suddenly becomes complicated with luminal thrombosis. If thrombosis-prone plaques could be detected and thrombosis averted, atherosclerosis would be a much more benign disease. Approximately 76% of all fatal coronary thrombi are precipitated by plaque rupture. Plaque rupture is a more frequent cause of coronary thrombosis in men (approximately 80%) than in women (approximately 60%). Ruptured plaques are characterized by a large lipid-rich core, a thin fibrous cap that contains few smooth muscle cells and many macrophages, angiogenesis, adventitial inflammation, and outward remodeling. Plaque rupture is the most common cause of coronary thrombosis. Ruptured plaques and, by inference, rupture-prone plaques have characteristic pathoanatomical features that might be useful for their detection in vivo by imaging. This article describes the pathogenesis of atherosclerosis, how it begets thrombosis, and the possibility to detect thrombosis-prone plaques and prevent heart attack.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The immunology of atherosclerosis

            Chronic kidney disease accelerates atherosclerosis via augmentation of inflammation, perturbation of lipid metabolism, and other mechanisms. Here, the authors describe the role of the immune system in the initiation and progression of atherosclerosis and discuss potential opportunities for therapy.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Lack of effect of long-term supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease.

              Observational studies suggest that people who consume more fruits and vegetables containing beta carotene have somewhat lower risks of cancer and cardiovascular disease, and earlier basic research suggested plausible mechanisms. Because large randomized trials of long duration were necessary to test this hypothesis directly, we conducted a trial of beta carotene supplementation. In a randomized, double-blind, placebo-controlled trial of beta carotene (50 mg on alternate days), we enrolled 22,071 male physicians, 40 to 84 years of age, in the United States; 11 percent were current smokers and 39 percent were former smokers at the beginning of the study in 1982. By December 31, 1995, the scheduled end of the study, fewer than 1 percent had been lost to follow-up, and compliance was 78 percent in the group that received beta carotene. Among 11,036 physicians randomly assigned to receive beta carotene and 11,035 assigned to receive placebo, there were virtually no early or late differences in the overall incidence of malignant neoplasms or cardiovascular disease, or in overall mortality. In the beta carotene group, 1273 men had any malignant neoplasm (except nonmelanoma skin cancer), as compared with 1293 in the placebo group (relative risk, 0.98; 95 percent confidence interval, 0.91 to 1.06). There were also no significant differences in the number of cases of lung cancer (82 in the beta carotene group vs. 88 in the placebo group); the number of deaths from cancer (386 vs. 380), deaths from any cause (979 vs. 968), or deaths from cardiovascular disease (338 vs. 313); the number of men with myocardial infarction (468 vs. 489); the number with stroke (367 vs. 382); or the number with any one of the previous three end points (967 vs. 972). Among current and former smokers, there were also no significant early or late differences in any of these end points. In this trial among healthy men, 12 years of supplementation with beta carotene produced neither benefit nor harm in terms of the incidence of malignant neoplasms, cardiovascular disease, or death from all causes.
                Bookmark

                Author and article information

                Journal
                Cells
                Cells
                cells
                Cells
                MDPI
                2073-4409
                01 March 2020
                March 2020
                : 9
                : 3
                : 584
                Affiliations
                [1 ]Institute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow 121609, Russia; sasha.melnichenko@ 123456gmail.com
                [2 ]Department of Internal Medicine, National Taiwan University Hospital, Bei-Hu Branch, Taipei 10617, Taiwan; weikaiwu0115@ 123456gmail.com
                [3 ]Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow 125315, Russia; nafany905@ 123456gmail.com
                [4 ]Clinic for Anesthesiology and Intensive Care Medicine, University Hospital Jena, Am Klinikum 1, D-07747 Jena, Germany; Reinhard.Wetzker@ 123456uni-jena.de
                [5 ]Institute of Human Morphology, Moscow 117418, Russia; vnsukhorukov@ 123456gmail.com (V.S.); alexander.markin.34@ 123456gmail.com (A.M.M.)
                Author notes
                [* ]Correspondence: tehhy_85@ 123456mail.ru (A.V.P.); a.h.opexob@ 123456gmail.com (A.N.O.)
                Author information
                https://orcid.org/0000-0002-9476-8998
                https://orcid.org/0000-0002-0312-3773
                https://orcid.org/0000-0003-2096-3237
                https://orcid.org/0000-0002-3318-4681
                Article
                cells-09-00584
                10.3390/cells9030584
                7140394
                32121535
                fd817ff4-260d-4762-b902-5f9583a3d1e5
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 27 December 2019
                : 25 February 2020
                Categories
                Review

                atherosclerosis,foam cells,cvd,ldl,modified ldl
                atherosclerosis, foam cells, cvd, ldl, modified ldl

                Comments

                Comment on this article