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Abstract
TRPA1, a nonselective cation channel, is expressed in sensory afferent that innervates peripheral targets. Neuronal TRPA1 can promote tissue repair, remove harmful stimuli and induce protective responses via the release of neuropeptides after the activation of the channel by chemical, exogenous, or endogenous irritants in the injured tissue. However, chronic inflammation after repeated noxious stimuli may result in the development of several diseases. In addition to sensory neurons, TRPA1, activated by inflammatory agents from some non-neuronal cells in the injured area or disease, might promote or protect disease progression. Therefore, TRPA1 works as a molecular sentinel of tissue damage or as an inflammation gatekeeper. Most kidney damage cases are associated with inflammation. In this review, we summarised the role of TRPA1 in neurogenic or non-neurogenic inflammation and in kidney disease, especially the non-neuronal TRPA1. In in vivo animal studies, TRPA1 prevented sepsis-induced or Ang-II-induced and ischemia-reperfusion renal injury by maintaining mitochondrial haemostasis or via the downregulation of macrophage-mediated inflammation, respectively. Renal tubular epithelial TRPA1 acts as an oxidative stress sensor to mediate hypoxia–reoxygenation injury in vitro and ischaemia–reperfusion-induced kidney injury in vivo through MAPKs/NF-kB signalling. Acute kidney injury (AKI) patients with high renal tubular TRPA1 expression had low complete renal function recovery. In renal disease, TPRA1 plays different roles in different cell types accordingly. These findings depict the important role of TRPA1 and warrant further investigation.
Highlights
transient receptor potential ankyrin 1 (TRPA1) channel activation by exogenous irritants, chemicals and proinflammatory agents is required for the release exogenous irritants, chemicals and proinflammatory agents is required for the release neuropeptides, such as substance P (SP), calcitonin gene-related peptide (CGRP) and ne of neuropeptides, such as substance P (SP), calcitonin gene-related peptide (CGRP) and rokinin A (NKA) [36,37] to promote and modulate inflammatory responses (Figure 2)
The TRPA1 channel is a molecular sentinel of tissue damage and an inflammation gatekeeper in both neuron and non-neuron cells
Kidney disease occurs due to tissue damage that is related to inflammation
Summary
Uremic toxins generated from high levels of metabolic end-products have become clinically relevant in CKD progression. These toxins are tightly related to many CKDassociated complications, such as hypertension, cardiovascular diseases, metabolic acidosis, anaemia, altered immune response, mineral and bone disturbances and neurological complications [6]. Cardiovascular dysfunctions and altered immune responses, which resulted in increased infections, have accounted for the risk of morbidity and mortality in CKD [7]. Inflammation and oxidative stresses play important roles in these conditions of CKD [8]. Patients with CKD typically suffer from chronic inflammation [9], and the dysfunction of the antioxidative systems worsens with the degree of renal function [10]. In this work we will provide a comprehensive review of our current knowledge on this ion channel relative to kidney diseases
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