Human macrophage pro-inflammatory polarization in response to free cholesterol and cholesterol remnants
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F25%3A00085642" target="_blank" >RIV/00023001:_____/25:00085642 - isvavai.cz</a>
Alternative codes found
RIV/00216208:11310/25:10499091
Result on the web
<a href="https://physoc.onlinelibrary.wiley.com/doi/epdf/10.14814/phy2.70367" target="_blank" >https://physoc.onlinelibrary.wiley.com/doi/epdf/10.14814/phy2.70367</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.14814/phy2.70367" target="_blank" >10.14814/phy2.70367</a>
Alternative languages
Result language
angličtina
Original language name
Human macrophage pro-inflammatory polarization in response to free cholesterol and cholesterol remnants
Original language description
Atherosclerosis is a chronic inflammatory disease of the blood vessels caused by elevated levels of lipoproteins. The hyperlipoproteinemia triggers a series of cellular changes, particularly the activation of the macrophages, which play a crucial role in the development and progression of atherosclerosis. The presence of free cholesterol (FC) in lipoproteins may contribute to macrophage stimulation. However, the mechanisms linking the accumulation of FC in macrophages to their pro-inflammatory activation remain poorly understood. Our research found a positive correlation between the number of pro-inflammatory macrophages (CD14 + CD16 + CD36high) in visceral adipose tissue and the levels of LDL-C and cholesterol remnant particles in 56 healthy people. In contrast, the proportion of anti-inflammatory, alternatively activated macrophages (CD14 + CD16-CD163+) correlated negatively with HDL-C. Additionally, our in vitro study demonstrated that macrophages accumulating FC promoted a pro-inflammatory response, activating the TNF-alpha and chemokine CCL3 genes. Furthermore, the accumulation of FC in macrophages alters the surface receptors on macrophages (CD206 and CD16) and increases cellular granularity. Notably, the CD36 surface receptor and the ACAT and CD36 genes did not show a response. These results suggest a link between excessive FC accumulation and systemic inflammation to underlie the development of atherosclerosis.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30105 - Physiology (including cytology)
Result continuities
Project
<a href="/en/project/LX22NPO5104" target="_blank" >LX22NPO5104: National Institute for Research of Metabolic and Cardiovascular Diseases</a><br>
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2025
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Physiological Reports
ISSN
2051-817X
e-ISSN
2051-817X
Volume of the periodical
13
Issue of the periodical within the volume
10
Country of publishing house
US - UNITED STATES
Number of pages
13
Pages from-to
"art. no. e70367"
UT code for WoS article
001493919900001
EID of the result in the Scopus database
2-s2.0-105006001692