Hypoxia enhances lipid uptake in macrophages: Role of the scavenger receptors Lox1, SRA, and CD36

Abstract

Hypoxia increases lipid uptake into macrophages and differentially regulates the expression of oxLDL receptors. Lox-1 plays a major role in hypoxia-induced foam cell formation which is, at least in part, mediated by HIF-1α.

Frailty predictors and outcomes among older patients with cardiovascular disease: Data from Fragicor

“…Additionally, the elevated rate of cardiovascular comorbidities (3 or more) in the frail group, suggests that they are more likely to have arterial diseases with inflammation, coagulation disorders and lower rates of peripheral oxygenation (Crucet et al, 2013;Parathath et al, 2011). The high frequency of HF in our sample (80%) may corroborate these findings.…”

Hypoxia-inducible factors: key regulators of myeloid cells during inflammation

“…Hypoxia has been implicated as a pathogenic factor in atherosclerosis and contributes to the proatherosclerotic functions of macrophages ( Figure 2A) (117). Several reports showed that lipid uptake and foam cell formation are dependent on hypoxia and HIF-1α (118)(119)(120). Both murine and human macrophage cell lines increase cellular neutral lipid content when cultured under hypoxic conditions; however, this effect is reversed upon HIF-1α depletion.…”

Protective role of n6/n3 PUFA supplementation with varying DHA/EPA ratios against atherosclerosis in mice

“…Obviously, foam cell formation is a key event in both early and late atherosclerotic lesions. It has been demonstrated that scavenger receptors A (SRA, also known as macrophage scavenger receptor 1, MSR1), lectin-like ox-LDL receptor (LOX-1), and cluster of differentiation 36 (CD36) are the most relevant for cholesterol uptake [25]. On the other hand, to prevent the accumulation of excess cholesterol, the esterification of cholesterol is mediated by the microsomal enzyme acyl-coenzyme A: cholesterol acyltransferase (ACAT) [26] and the efflux of cholesterol or reverse cholesterol transport is regulated by the transporters ATP binding cassette transporter A1 (ABCA1), ATP binding cassette transporter G1 (ABCG1) [27,28].…”