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This review highlights pip5k1α's involvement in asthma mechanisms, suggesting potential therapeutic strategies for airway hyper-responsiveness and immune homeostasis.
PIP5K1α is a key member of the lipid kinase family, involved in several cellular processes including cell proliferation and differentiation, cytoskeletal remodeling, inositol-phospholipid signaling, intracellular vesicle transport, and protein secretion. Emerging evidence now highlights critical functions of PIP5K1α in asthma-related biological processes. In this review, we aim to consolidate existing literature on the involvement of PIP5K1α in asthma pathogenesis. We summarize PIP5K1α-related pathways that regulate airway immune homeostasis (regulating T cell/ILCs-mediated immune response, TLR4/MyD88/NF-κB signaling pathway, Let-7 miRNA biogenesis, and its regulatory modifications), airway hyper-responsiveness (modulating of calcium release, airway smooth muscle contractility, and epithelial barrier dysfunction), and airway remodeling (regulating cell migration, proliferation, epithelial remodeling, and cytoskeleton modulation) in asthma. Although clinically approved PIP5K1α inhibitors are currently unavailable, targeting this kinase present a compelling therapeutic strategy for asthma, requiring further research into develop effective treatments.
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Wang et al. (2025) studied this question.
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