ArticleCell death & disease2026
SREBP2 promotes macrophage alternative activation and allergic airway inflammation independent of cholesterol biosynthesis.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Lipid droplet-mitochondria contact sites as druggable spatial-pharmacology targets in respiratory disease: cross-cell-type mechanisms and translational strategies.Frontiers in cell and developmental biology · 2026Review
- Systemic immune programming in the life course of childhood asthma: a new perspective on monocyte pre-activation and trained immunity.Frontiers in immunology · 2026Review
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Authors and funding
15 authors.
Funding
Abstract
Immunometabolic reprogramming is increasingly recognized as a critical regulator of macrophage activation and function. This study aimed to elucidate the role of the SREBP2-cholesterol biosynthetic pathway in M2 activation of interstitial macrophages (IMs) during allergic asthma. We observed a significant expansion of M2-polarized IMs with heightened SREBP2-cholesterol biosynthetic activity in the lungs of asthmatic mice. IL4, a key pro-allergic cytokine in allergic asthma, was found to induce SREBP2 maturation and activate the cholesterol biosynthetic signaling pathway in macrophages. Moreover, inhibiting SREBP2 maturation restrains IL4-induced M2 activation, both in vitro and in vivo. Intriguingly, this effect was independent of intracellular cholesterol levels; instead, cholesterol itself negatively regulated SREBP2 maturation and M2 activation. Mechanistically, mature SREBP2 transcriptional modulated IRF4 expression and interacted with it to promote IL4-induced M2 activation. Additionally, myeloid-specific Scap deficiency impeded the SREBP2 maturation process in macrophages, leading to reduced M2 activation and allergic airway inflammation. These findings highlight the pivotal role of the SREBP2-IRF4 axis in modulating M2 polarization of IMs and suggest potential therapeutic targets for asthma treatment.
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