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Pathomechanisms of Atherosclerosis. Part III

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 9091

Special Issue Editor

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue "Pathomechanisms of Atherosclerosis. Part II".

With the recent globalisation of lifestyle in many parts of the world, atherosclerosis has become a global disease posing a significant health threat and economic burden, not only in the West, but now also Asia and Africa. Despite the well-documented conventional risk factors for atherosclerosis, little is known about the major differences between geographical regions and whether the effect of those factors has a similar level of impact in all nations. This also raises questions about the exact pathomechanism of atherosclerosis and whether it is uniform or if it may have different pathways between continents and countries. Furthermore, whether the pattern of gross pathology (e.g., thickened intima-media, plaque formation, calcification, etc.) has become amenable to study and accurate analysis is not known; is it nation specific?

This Special Issue of IJMS searches for answers to some of the abovementioned questions in an attempt to provide cardiology and vascular specialists with some answers that should lead to a better understanding of this serious universal disease. We look forward to your contributions.

Prof. Dr. Michael Henein
Guest Editor

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Keywords

  • atherosclerosis
  • coronary calcification
  • arterial disease
  • inflammation
  • pathomechanism of atherosclerosis

Published Papers (2 papers)

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Review

17 pages, 866 KiB  
Review
The Emerging Roles of Chromogranins and Derived Polypeptides in Atherosclerosis, Diabetes, and Coronary Heart Disease
by Takuya Watanabe
Int. J. Mol. Sci. 2021, 22(11), 6118; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22116118 - 06 Jun 2021
Cited by 15 | Viewed by 4488
Abstract
Chromogranin A (CgA), B (CgB), and C (CgC), the family members of the granin glycoproteins, are associated with diabetes. These proteins are abundantly expressed in neurons, endocrine, and neuroendocrine cells. They are also present in other areas of the body. Patients with diabetic [...] Read more.
Chromogranin A (CgA), B (CgB), and C (CgC), the family members of the granin glycoproteins, are associated with diabetes. These proteins are abundantly expressed in neurons, endocrine, and neuroendocrine cells. They are also present in other areas of the body. Patients with diabetic retinopathy have higher levels of CgA, CgB, and CgC in the vitreous humor. In addition, type 1 diabetic patients have high CgA and low CgB levels in the circulating blood. Plasma CgA levels are increased in patients with hypertension, coronary heart disease, and heart failure. CgA is the precursor to several functional peptides, including catestatin, vasostatin-1, vasostatin-2, pancreastatin, chromofungin, and many others. Catestatin, vasostain-1, and vasostatin-2 suppress the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 in human vascular endothelial cells. Catestatin and vasostatin-1 suppress oxidized low-density lipoprotein-induced foam cell formation in human macrophages. Catestatin and vasostatin-2, but not vasostatin-1, suppress the proliferation and these three peptides suppress the migration in human vascular smooth muscles. Chronic infusion of catestatin, vasostatin-1, or vasostatin-2 suppresses the development of atherosclerosis of the aorta in apolipoprotein E-deficient mice. Catestatin, vasostatin-1, vasostatin-2, and chromofungin protect ischemia/reperfusion-induced myocardial dysfunction in rats. Since pancreastatin inhibits insulin secretion from pancreatic β-cells, and regulates glucose metabolism in liver and adipose tissues, pancreastatin inhibitor peptide-8 (PSTi8) improves insulin resistance and glucose homeostasis. Catestatin stimulates therapeutic angiogenesis in the mouse hind limb ischemia model. Gene therapy with secretoneurin, a CgC-derived peptide, stimulates postischemic neovascularization in apolipoprotein E-deficient mice and streptozotocin-induced diabetic mice, and improves diabetic neuropathy in db/db mice. Therefore, CgA is a biomarker for atherosclerosis, diabetes, hypertension, and coronary heart disease. CgA- and CgC--derived polypeptides provide the therapeutic target for atherosclerosis and ischemia-induced tissue damages. PSTi8 is useful in the treatment of diabetes. Full article
(This article belongs to the Special Issue Pathomechanisms of Atherosclerosis. Part III)
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13 pages, 2054 KiB  
Review
Macrophage Function and the Role of GSK3
by Sarvatit Patel and Geoff H. Werstuck
Int. J. Mol. Sci. 2021, 22(4), 2206; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22042206 - 23 Feb 2021
Cited by 15 | Viewed by 3646
Abstract
Macrophages are present in nearly all vertebrate tissues, where they respond to a complex variety of regulatory signals to coordinate immune functions involved in tissue development, metabolism, homeostasis, and repair. Glycogen synthase kinase 3 (GSK3) is a ubiquitously expressed protein kinase that plays [...] Read more.
Macrophages are present in nearly all vertebrate tissues, where they respond to a complex variety of regulatory signals to coordinate immune functions involved in tissue development, metabolism, homeostasis, and repair. Glycogen synthase kinase 3 (GSK3) is a ubiquitously expressed protein kinase that plays important roles in multiple pathways involved in cell metabolism. Dysregulation of GSK3 has been implicated in several prevalent metabolic disorders, and recent findings have highlighted the importance of GSK3 activity in the regulation of macrophages, especially with respect to the initiation of specific pathologies. This makes GSK3 a potential therapeutic target for the development of novel drugs to modulate immunometabolic responses. Here, we summarize recent findings that have contributed to our understanding of how GSK3 regulates macrophage function, and we discuss the role of GSK3 in the development of metabolic disorders and diseases. Full article
(This article belongs to the Special Issue Pathomechanisms of Atherosclerosis. Part III)
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