Curcumin as a potential modulator of M1 and M2 macrophages: new insights in atherosclerosis therapy.

Abstract:

:Accumulation of macrophages within the artery wall is an eminent feature of atherosclerotic plaques. Macrophages are influenced by various plaque microenvironmental stimuli, such as oxidized lipids, cytokines, and senescent erythrocytes, and thereby polarize into two main phenotypes called proinflammatory M1 and anti-inflammatory M2 macrophages. In the hemorrhagic zones of atheroma, upon exposure to iron, sequestration of iron by M1 macrophages results in an uncontrolled proinflammatory phenotype impairing wound healing, while M2 macrophages phagocytose both apoptotic cells and senescent erythrocytes. M1 macrophages are prominent phenotype in the unstable plaques, in which plaque shoulder contains macrophages mainly present markers of M1 phenotype, whereas the fibrous cap encompassing the necrotic lipid core content macrophages expressed markers of both M1 and M2 subtypes. The abovementioned findings suggest macrophage modulation as a potent approach for atherosclerosis therapy. Curcumin is a polyphenol dietary derived from turmeric with numerous pharmacological activities. Recent in vitro and in vivo studies have indicated that curcumin exerted lipid-lowering effects, and also can modulate function of different macrophage subsets in various macrophage-involved diseases. The current review aimed to present role of macrophage subtypes in atherosclerosis development and progression, and to understand effect of curcumin on macrophage polarization and foam cell formation in the atherosclerosis lesions. Overall, we would address important targets for macrophage modulation in atherosclerotic plaques.

journal_name

Heart Fail Rev

journal_title

Heart failure reviews

authors

Momtazi-Borojeni AA,Abdollahi E,Nikfar B,Chaichian S,Ekhlasi-Hundrieser M

doi

10.1007/s10741-018-09764-z

subject

Has Abstract

pub_date

2019-05-01 00:00:00

pages

399-409

issue

3

eissn

1382-4147

issn

1573-7322

pii

10.1007/s10741-018-09764-z

journal_volume

24

pub_type

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