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Context-dependent lysophosphatidic acid signalling in inflammation: evidence hierarchy, myeloid regulation and translational gaps
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DOI：10.1007/s00011-026-02337-z.png)
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Abstract
En 中文
Lysophosphatidic acid (LPA) has been extensively reviewed in receptor pharmacology, fibrosis, cancer, vascular biology and neural injury. Its role in inflammation remains difficult to interpret because well-replicated pathogenic or pro-remodelling actions coexist with selected macrophage-regulatory effects reported under defined experimental conditions. This structured narrative review provides an evidence-weighted framework for interpreting these divergent findings. The strongest evidence supports LPA as an injury- and remodelling-associated signal in vascular–stromal programmes, pain-associated settings and tumour immune escape. By contrast, LPA-mediated attenuation of selected LPS/TLR4-driven macrophage responses is biologically plausible but incompletely replicated and receptor-divergent. The more specific LPAR1-dependent model of M2-like and metabolic macrophage reprogramming remains less independently validated, especially in primary human myeloid cells and physiologically plausible concentration ranges. LPA should not be classified as simply pro-inflammatory or anti-inflammatory. Anti-inflammatory LPA models should be regarded as experimentally plausible but translationally unproven until validated using defined LPA species, receptor-resolved perturbation and concentration-resolved human myeloid-cell systems.
Keywords:
Lysophosphatidic acid
Autotaxin
LPA receptor
Macrophage
Microglia
Immunometabolism
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