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The role of iron in the pathogenesis of atherosclerosis

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11120%2F17%3A43913154" target="_blank" >RIV/00216208:11120/17:43913154 - isvavai.cz</a>

  • Alternative codes found

    RIV/00064173:_____/17:N0000110

  • Result on the web

    <a href="http://www.biomed.cas.cz/physiolres/pdf/66/66_S55.pdf" target="_blank" >http://www.biomed.cas.cz/physiolres/pdf/66/66_S55.pdf</a>

  • DOI - Digital Object Identifier

Alternative languages

  • Result language

    angličtina

  • Original language name

    The role of iron in the pathogenesis of atherosclerosis

  • Original language description

    Ferritin and increased iron stores first appeared on the list of cardiovascular risk factors more than 30 years ago and their causal role in the pathogenesis of atherosclerosis has been heavily discussed since the early 1990s. It seems that besides traditional factors such as hyperlipoproteinemia, hypertension, diabetes mellitus, obesity, physical inactivity, smoking and family history, high iron stores represent an additional parameter that could modify individual cardiovascular risk. The role of iron in the pathogenesis of atherosclerosis was originally primarily associated with its ability to catalyze the formation of highly reactive free oxygen radicals and the oxidation of atherogenic lipoproteins. Later, it became clear that the mechanism is more complex. Atherosclerosis is a chronic fibroproliferative inflammatory process and iron, through increased oxidation stress as well as directly, can control both native and adaptive immune responses. Within the arterial wall, iron affects all of the cell types that participate in the atherosclerotic process (monocytes/macrophages, endothelial cells, vascular smooth muscle cells and platelets). Most intracellular iron is bound in ferritin, whereas redox-active iron forms labile iron pool. Pro-inflammatory and anti-inflammatory macrophages within arterial plaque differ with regard to the amount of intracellular iron and most probably with regard to their labile iron pool. Yet, the relation between plasma ferritin and intracellular labile iron pool has not been fully clarified. Data from population studies document that the consumption of meat and lack of physical activity contribute to increased iron stores. Patients with hereditary hemochromatosis, despite extreme iron storage, do not show increased manifestation of atherosclerosis probably due to the low expression of hepcidin in macrophages.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30202 - Endocrinology and metabolism (including diabetes, hormones)

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2017

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Physiological Research

  • ISSN

    0862-8408

  • e-ISSN

  • Volume of the periodical

    66

  • Issue of the periodical within the volume

    Suppl. 1

  • Country of publishing house

    CZ - CZECH REPUBLIC

  • Number of pages

    13

  • Pages from-to

    "S55"-"S67"

  • UT code for WoS article

    000398620900007

  • EID of the result in the Scopus database

    2-s2.0-85017179610