Transient receptor potential channels in pulmonary chemical injuries and as countermeasure targets.
Transient receptor potential channels in pulmonary chemical injuries and as countermeasure targets.
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DOI：
10.1111/nyas.14472
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发表时间：
2020-11
影响因子：
5.2
通讯作者：
Jordt SE
中科院分区：
文献类型：
--
作者：
Achanta S;Jordt SE
肺对工业或运输事故、职业暴露或故意用作大规模杀伤性武器（WMD）中的威胁剂造成的化学损伤高度敏感。大多数化学威胁剂和有毒吸入危害物（TIH）尽管作为大规模毁灭性武器使用了世纪，但没有解毒剂。在几个假定的目标，瞬时受体电位（TRP）离子通道作为介质的各种吸入化学威胁剂的损伤的证据正在出现。TRP通道在呼吸系统中表达，对体内平衡至关重要。在TRP通道中，大量文献支持TRPA1、TRPV1和TRPV4在肺化学损伤中的重要作用。TRP通道通过感觉神经元和非神经元途径介导其功能。TRP通道在复杂的肺病理生理事件中起关键作用，包括但不限于细胞内钙水平升高、信号转导、促炎细胞募集、神经源性炎症途径、咳嗽反射、粘液清除受阻、上皮完整性破坏、肺水肿和纤维化。在这篇综述中，我们总结了TRP通道在化学威胁剂引起的肺损伤中的作用，以及这些通道如何作为更广泛适应症的医学对策目标。
The lung is highly sensitive to chemical injuries caused by exposure to threat agents in industrial or transportation accidents, occupational exposures, or deliberate use as weapons of mass destruction (WMD). There are no antidotes for the majority of the chemical threat agents and toxic inhalation hazards (TIH) despite their use as WMDs for more than a century. Among several putative targets, evidence for transient receptor potential (TRP) ion channels as mediators of injury by various inhalational chemical threat agents is emerging. TRP channels are expressed in the respiratory system and are essential for homeostasis. Among TRP channels, the body of literature supporting essential roles for TRPA1, TRPV1, and TRPV4 in pulmonary chemical injuries is abundant. TRP channels mediate their function through sensory neuronal and non-neuronal pathways. TRP channels play a crucial role in complex pulmonary pathophysiologic events including, but not limited to, increased intracellular calcium levels, signal transduction, recruitment of proinflammatory cells, neurogenic inflammatory pathways, cough reflex, hampered mucus clearance, disruption of the integrity of the epithelia, pulmonary edema, and fibrosis. In this review, we summarize the role of TRP channels in chemical threat agents–induced pulmonary injuries and how these channels may serve as medical countermeasure targets for broader indications.
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DOI：
10.1513/pats.201001-004sm
发表时间：
2010-07-01
期刊：
Proceedings of the American Thoracic Society
影响因子：
--
作者：
Bessac, Bret F;Jordt, Sven-Eric
通讯作者：
Jordt, Sven-Eric
影响因子：
15.9
作者：
Bessac, Bret F.;Sivula, Michael;Jordt, Sven-Eric
通讯作者：
Jordt, Sven-Eric
DOI：
10.1152/physiol.00026.2008
发表时间：
2008-12
期刊：
Physiology (Bethesda, Md.)
影响因子：
--
作者：
Bessac BF;Jordt SE
通讯作者：
Jordt SE
影响因子：
3.5
作者：
Andres D;Keyser B;Benton B;Melber A;Olivera D;Holmes W;Paradiso D;Anderson D;Ray R
通讯作者：
Ray R
影响因子：
4.3
作者：
Balte, Pallavi P.;Clark, Kathleen A.;Svendsen, Erik R.
通讯作者：
Svendsen, Erik R.