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Review
. 2024 May 22;13(11):889.
doi: 10.3390/cells13110889.

Lipid-Laden Macrophages in Pulmonary Diseases

Yin Zhu  1   2 , Dooyoung Choi  1 , Payaningal R Somanath  1   2   3 , Duo Zhang  1   2   3
Affiliations
Review

Lipid-Laden Macrophages in Pulmonary Diseases

Yin Zhu et al. Cells. .

Abstract

Pulmonary surfactants play a crucial role in managing lung lipid metabolism, and dysregulation of this process is evident in various lung diseases. Alternations in lipid metabolism lead to pulmonary surfactant damage, resulting in hyperlipidemia in response to lung injury. Lung macrophages are responsible for recycling damaged lipid droplets to maintain lipid homeostasis. The inflammatory response triggered by external stimuli such as cigarette smoke, bleomycin, and bacteria can interfere with this process, resulting in the formation of lipid-laden macrophages (LLMs), also known as foamy macrophages. Recent studies have highlighted the potential significance of LLM formation in a range of pulmonary diseases. Furthermore, growing evidence suggests that LLMs are present in patients suffering from various pulmonary conditions. In this review, we summarize the essential metabolic and signaling pathways driving the LLM formation in chronic obstructive pulmonary disease, pulmonary fibrosis, tuberculosis, and acute lung injury.

Keywords: COPD; lipid accumulation; lipid-laden macrophage; pulmonary fibrosis; reactive oxygen species; tuberculosis.

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Conflict of interest statement

The authors declare that there are no conflicts of interest.

Figures

Figure 1
Figure 1
Schematic diagrams of signaling pathways regulate LLM formation in pulmonary diseases. The lung injury caused by external stimuli disrupts lipid metabolism, leading to damage to the pulmonary surfactant and an increase in reactive oxygen species (ROS) levels. The inflammatory cytokines that are released increase the expression of scavenger receptors (SRs), cluster of differentiation 36 (CD36), liver X receptors (LXRs), and low-density lipoprotein receptor (LDLR), which enables the transport of damaged or oxidized lipid droplets within macrophages. As the lipid levels within the cell rise, the activity of ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette subfamily G member 1 (ABCG1) is suppressed, while transforming growth factor-beta (TGFβ) and peroxisome proliferator-activated receptor γ (PPARγ) further contribute to the accumulation of lipids.
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