Exercise for slowing the progression of atherosclerotic process: effects on inflammatory markers

2021 ◽  
Vol 63 (2) ◽  
Author(s):  
Crescenzo TESTA ◽  
Anna DI LORENZO ◽  
Alessandro PARLATO ◽  
Giuseppe D’AMBROSIO ◽  
Aurora MEROLLA ◽  
...  
2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Giuseppina T. Russo ◽  
Annalisa Giandalia ◽  
Elisabetta L. Romeo ◽  
Angela Alibrandi ◽  
Katalin V. Horvath ◽  
...  

Background. Besides their role in reverse cholesterol transport, HDL particles may affect the atherosclerotic process through the modulation of subclinical inflammation. HDL particles differ in size, composition, and, probably, anti-inflammatory properties. This hypothesis has never been explored in diabetic women, frequently having dysfunctional HDL. The potential relationship between lipid profile, Apo-AI containing HDL subclasses distribution, and common inflammatory markers (hsCRP, IL-6) was examined in 160 coronary heart disease- (CHD-) free women with and without type 2 diabetes.Results. Compared to controls, diabetic women showed lower levels of the atheroprotective large α-1, α-2, and pre-α-1 and higher concentration of the small, lipid-poor α-3 HDL particles (P<0.05all); diabetic women also had higher hsCRP and IL-6 serum levels (age- and BMI-adjustedP<0.001). Overall, HDL subclasses significantly correlated with inflammatory markers: hsCRP inversely correlated with α-1(P=0.01)and pre-α-1(P=0.003); IL-6 inversely correlated with α-1(P=0.003), α-2(P=0.004), and pre-α-1(P=0.002)and positively with α-3 HDL(P=0.03). Similar correlations were confirmed at univariate regression analysis.Conclusions. More atheroprotective HDL subclasses are associated with lower levels of inflammatory markers, especially in diabetic women. These data suggest that different HDL subclasses may influence CHD risk also through the modulation of inflammation.


PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-7 ◽  
Author(s):  
Ana Z. Fernandez

Inflammation has been recognized as an important hallmark of atherosclerosis. The pharmacological activation of PPAR- by the thiazolidinediones in diabetes, and of PPAR- by the fibrates in hyperlipidemia has been shown to help to reduce inflammatory markers in preclinical and clinical studies. PPARs are known to modulate immune pathways through at least three different mechanisms: by direct binding to PPRE of anti-inflammatory cytokines genes; by transrepression of transcription factors like NF-B and AP-1; or by corepression. The regulation of the inflammatory pathways by PPARs can be achieved on each one of the cells involved in the atherosclerotic process, that is, monocytes, macrophages, T cells, endothelial cells, and smooth muscle cells. Moreover, as each of these cellular components is interconnected with each other, PPAR activation in one cell type could affect the other ones. As activation of PPARs has clear ant-inflammatory benefits, PPARs ligands should be considered as a new therapeutical approach to ameliorate the exacerbated immune response in atherosclerotic diseases.


2007 ◽  
Vol 6 (1) ◽  
pp. 154-154
Author(s):  
A KALOGEROPOULOS ◽  
A RIGOPOULOS ◽  
S PAPATHANASIOU ◽  
S TSIODRAS ◽  
S DRAGOMANOVITS ◽  
...  

2006 ◽  
Vol 36 (21) ◽  
pp. 9
Author(s):  
STEPHEN STICK ◽  
SIMON GODFREY
Keyword(s):  

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