Tuning macrophages for atherosclerosis treatment

Abstract

Atherosclerosis is a chronic inflammatory vascular disease and one of the leading causes of death worldwide. Macrophages play an important role in atherosclerosis in the inflammatory response, cell-cell communications, plaque growth, and plaque rupture in atherosclerotic lesions. Here we review the sources, functions, and complex phenotypes of macrophages in the progression of atherosclerotic, and discuss the recent approaches in modulating macrophage autophagy and phenotypic transformation for atherosclerosis treatment. We then focus on the drug delivery strategies that target macrophages or use macrophage membrane-coated particles to deliver therapeutics to the lesion sites. These biomaterial-based approaches to target, modulate, or engineer macrophages have broad applications for disease therapies and tissue regeneration.

Identification of co-expressed central genes and transcription factors in acute myocardial infarction and diabetic nephropathy

“…Atherosclerosis is a chronic inflammatory vascular disease [ 33 ]; both AMI and DN are essentially atherosclerotic diseases; and most immune cells are involved in the atherosclerotic process [ 34 ]. Macrophages are considered the main immune cell type in atherosclerotic plaques [ 35 ], acting as antigen-presenting cells and presenting antigens to naive CD8 + T cells and naive CD4 + T cells [ 36 ]. CD8 + killer T cells induce apoptosis and necrosis of target cells, exacerbating progression in atherosclerotic plaques [ 37 ], while CD4T cell subsets can influence atherosclerotic progression through immune activation or immunosuppression [ 38 ].…”

The Nutritional Intervention of Ingredients from Food Medicine Homology Regulating Macrophage Polarization on Atherosclerosis

“…In the early phase of atherosclerosis, cholesterol deposits in vascular tissue are eliminated via autophagy. 54 After IFMH intervention, LC3-II expression increased, whereas P62 expression decreased, indicating that autophagy increased in cells.…”

“…IFMH protects against atherosclerosis by decreasing ox-LDL-stimulated macrophage lipid accumulation and suppressing foam cell formation. In the early phase of atherosclerosis, cholesterol deposits in vascular tissue are eliminated via autophagy . After IFMH intervention, LC3-II expression increased, whereas P62 expression decreased, indicating that autophagy increased in cells.…”

Moxibustion's protective role against atherosclerosis: Inhibition of Ca2+ overload‐triggered oxidative stress and inflammatory response via P2Y12/PI3K/AKT pathway

“…4 Frequently classified as a macrophage subtype, foam cells exhibit persistent residence within plaques, thereby contributing to the disease's progression. 5 Intracellular Ca 2+ overload in macrophages is identified as a powerful stimulant for oxidative stress and inflammatory responses, which in turn, aggravate atherosclerotic plaque formation and advancement. 6 Consequently, the assessment of intracellular Ca 2+ concentrations is fundamentally crucial to comprehend the pathophysiological mechanisms underpinning atherosclerosis development.…”

“…Frequently classified as a macrophage subtype, foam cells exhibit persistent residence within plaques, thereby contributing to the disease's progression 5 . Intracellular Ca 2+ overload in macrophages is identified as a powerful stimulant for oxidative stress and inflammatory responses, which in turn, aggravate atherosclerotic plaque formation and advancement 6 .…”