Scholarlink

<p>Although prevalent in critical care, sepsis-associated acute lung injury (sALI) lacks a clear mechanistic framework and disease-modifying therapies. In this narrative review, we synthesize clinical and experimental data implicating lipid mediators (LMs) as underappreciated drivers of pulmonary barrier failure in sALI. LMs are known activators or sensitizers of transient receptor potential (TRP) channels expressed in non-neuronal lung cells. In endothelial and epithelial compartments, activation of TRP channels elevates intracellular Ca²⁺, increases microvascular permeability, impairs alveolar fluid clearance, and promotes pulmonary edema. Converging metabolomic and translational studies associate accumulation of specific LMs with respiratory failure, providing a mechanistic link between the LMs and TRP-dependent barrier dysfunction. We propose the activation of TRP channels by LMs as a key underlying mechanism of sALI. Clarifying this mechanism, biomarker-guided studies may enable more targeted clinical trials and ultimately improve outcomes in sALI.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Sepsis-associated acute lung injury: do inflammatory lipid mediators flood the lungs by activating pulmonary TRP channels?

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月17日

查看全文
  • Nada Birkic,
  • Robert R. Ehrman,
  • Đurđica Cekinović Grbeša,
  • Zeljka Minic,
  • Christian A. Reynolds

摘要

Although prevalent in critical care, sepsis-associated acute lung injury (sALI) lacks a clear mechanistic framework and disease-modifying therapies. In this narrative review, we synthesize clinical and experimental data implicating lipid mediators (LMs) as underappreciated drivers of pulmonary barrier failure in sALI. LMs are known activators or sensitizers of transient receptor potential (TRP) channels expressed in non-neuronal lung cells. In endothelial and epithelial compartments, activation of TRP channels elevates intracellular Ca²⁺, increases microvascular permeability, impairs alveolar fluid clearance, and promotes pulmonary edema. Converging metabolomic and translational studies associate accumulation of specific LMs with respiratory failure, providing a mechanistic link between the LMs and TRP-dependent barrier dysfunction. We propose the activation of TRP channels by LMs as a key underlying mechanism of sALI. Clarifying this mechanism, biomarker-guided studies may enable more targeted clinical trials and ultimately improve outcomes in sALI.