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September 10, 2025Journal of Translational Medicine1 citationsOpen Access

Implicates of PIP5K1α in asthma-related biological processes: insights into mechanisms and therapeutic potential

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SWSijia WangChinese Academy of SciencesFYFuwen YuanDuke UniversityLYLei-Miao YinShanghai University of Traditional Chinese Medicine

Key Points

  • PIP5K1α plays a critical role in asthma-related biological processes.
  • This review consolidates literature on PIP5K1α involvement in airway immune homeostasis, airway hyper-responsiveness, and airway remodeling.
  • Critical pathways related to PIP5K1α influence T cell responses, calcium release, and epithelial dysfunction.
  • Targeting PIP5K1α may present a novel therapeutic strategy for asthma; further research is needed.

Abstract

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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Cite This Study

Wang et al. (2025) studied this question.

synapsesocial.com/papers/68c182609b7b07f3a060f386https://doi.org/10.1186/s12967-025-06997-z
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