Abstract
The transient receptor potential ankyrin 1 (TRPA1) channel is a calcium-permeable nonselective cation channel in the plasma membrane that belongs to the transient receptor potential (TRP) channel superfamily. Recent studies have suggested that the TRPA1 channel plays an essential role in the development and progression of several cardiovascular conditions, such as atherosclerosis, heart failure, myocardial ischemia–reperfusion injury, myocardial fibrosis, arrhythmia, vasodilation, and hypertension. Activation of the TRPA1 channel has a protective effect against the development of atherosclerosis. Furthermore, TRPA1 channel activation elicits peripheral vasodilation and induces a biphasic blood pressure response. However, loss of channel expression or blockade of its activation suppressed heart failure, myocardial ischemia–reperfusion injury, myocardial fibrosis, and arrhythmia. In this paper, we review recent research progress on the TRPA1 channel and discuss its potential role in the cardiovascular system.
Highlights
The mammalian transient receptor potential (TRP) superfamily of cation channels has six subfamilies, including the vanilloid (TRPV), canonical (TRPC), melastatin (TRPM), ankyrin (TRPA), polycystin (TRPP), and mucolipin (TRPML) subfamilies, which are separated based on sequence homology (Venkatachalam and Montell, 2007)
We summarize the potential involvement of the transient receptor potential ankyrin 1 (TRPA1) channel in modulating pathophysiologic conditions, including atherosclerosis, heart failure, myocardial ischemia–reperfusion injury (IRI), myocardial fibrosis, arrhythmia, vasodilation, and hypertension (Table 3)
The current review described the potential role of the TRPA1 channel in the regulation of the cardiovascular system
Summary
The mammalian transient receptor potential (TRP) superfamily of cation channels has six subfamilies, including the vanilloid (TRPV), canonical (TRPC), melastatin (TRPM), ankyrin (TRPA), polycystin (TRPP), and mucolipin (TRPML) subfamilies, which are separated based on sequence homology (Venkatachalam and Montell, 2007). The TRPA1 channel responds to a wide range of agonists, including pungent natural compounds, such as allyl isothiocyanate (AITC), cinnamaldehyde, and allicin (Bandell et al, 2004; Jordt et al, 2004; Macpherson et al, 2005); ambient toxins, such as acrolein and nicotine (Andre et al, 2008; Talavera et al, 2009); anesthetic agents, such as propofol and lidocaine (Leffler et al, 2011; Woll et al, 2017); chemical compounds, such as ASP-7663 and optovin (Kokel et al, 2013; Kojima et al, 2014); and a range of endogenous agonists, such as oxidized lipids, nitric oxide (NO), and hydrogen sulfide (H2S) (Andersson et al, 2008; Eberhardt et al, 2014) Both intracellular and extracellular Ca2+ can directly activate the channel, whose activation can be further strengthened by agonists (Zurborg et al, 2007; Wang et al, 2008). We summarize the potential involvement of the TRPA1 channel in modulating pathophysiologic conditions, including atherosclerosis, heart failure, myocardial ischemia–reperfusion injury (IRI), myocardial fibrosis, arrhythmia, vasodilation, and hypertension (Table 3)
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