Monocyte CD36 expression associates with atherosclerotic burden in diabetes mellitus

Chandran, Jayanthi; Wadhwa, Neelam; Madhu, Sri Venkata; Kumar, Rajive; Sharma, Satendra

doi:10.1016/j.diabres.2020.108156

Cited by 7 publications

(1 citation statement)

References 19 publications

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“…As mentioned above, atherosclerotic plaques have high lipoprotein and oxidized lipid contents, which strongly induce macrophage inflammatory activation and lipid uptake by CD36 and LPL activities [ 23 , 70 , 76 , 77 ] . In diabetic patients, high serum CD36 levels have long been associated with insulin resistance and hyperglycemia, and recently, its expression in circulating monocytes has been strongly correlated with poor glycemic control and coronary artery disease risk in diabetic subjects [ 78 , 79 ] . In mice, specific bone marrow cell deletion of CD36 and LPL decreased plaque size and foam cell number (a common characteristic of advanced plaques) by reducing macrophage FA accumulation, demonstrating that targeting lipid uptake may be a therapeutic strategy to prevent macrophage dysfunction [ 23 , 70 , 76 , 77 ] .…”

Section: Macrophage Metabolism In Atherosclerosismentioning

confidence: 99%

Macrophage immunometabolism in diabetes-associated atherosclerosis

Gindri dos Santos,

Goedeke

2023

Immunometabolism

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Macrophages play fundamental roles in atherosclerotic plaque formation, growth, and regression. These cells are extremely plastic and perform different immune functions depending on the stimuli they receive. Initial in vitro studies have identified specific metabolic pathways that are crucial for the proper function of pro-inflammatory and pro-resolving macrophages. However, the plaque microenvironment, especially in the context of insulin resistance and type 2 diabetes, constantly challenges macrophages with several simultaneous inflammatory and metabolic stimuli, which may explain why atherosclerosis is accelerated in diabetic patients. In this mini review, we discuss how macrophage mitochondrial function and metabolism of carbohydrates, lipids, and amino acids may be affected by this complex plaque microenvironment and how risk factors associated with type 2 diabetes alter the metabolic rewiring of macrophages and disease progression. We also briefly discuss current challenges in assessing macrophage metabolism and identify future tools and possible strategies to alter macrophage metabolism to improve treatment options for diabetes-associated atherosclerosis.

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