TRPA1 as Target in Myocardial Infarction

Transient receptor potential cation channel subfamily A member 1 (TRPA1), an ion channel primarily expressed on sensory neurons, can be activated by substances occurring during myocardial infarction. Aims were to investigate whether activation, inhibition, or absence of TRPA1 affects infarcts and to...

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Bibliographic Details
Published in:International journal of molecular sciences 2023-01, Vol.24 (3), p.2516
Main Authors: Hoebart, Clara, Kiss, Attila, Pilz, Patrick M, Szabo, Petra L, Podesser, Bruno K, Fischer, Michael J M, Heber, Stefan
Format: Article
Language:English
Subjects:
Animals
Cardiomyocytes
Coronary vessels
Experiments
Heart attacks
Hypoxia
Ischemia
Mice
Mice, Knockout
Myocardial infarction
Myocardial Infarction - genetics
Myocardium
Neurons
Rats
Reperfusion
reperfusion-injury
Sensory neurons
Sensory Receptor Cells
Transient Receptor Potential Channels - genetics
Transient receptor potential proteins
TRPA1 Cation Channel - genetics
Veins & arteries
Citations: Items that this one cites
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Summary:Transient receptor potential cation channel subfamily A member 1 (TRPA1), an ion channel primarily expressed on sensory neurons, can be activated by substances occurring during myocardial infarction. Aims were to investigate whether activation, inhibition, or absence of TRPA1 affects infarcts and to explore underlying mechanisms. In the context of myocardial infarction, rats received a TRPA1 agonist, an antagonist, or vehicle at different time points, and infarct size was assessed. Wild type and TRPA1 knockout mice were also compared in this regard. In vitro, sensory neurons were co-cultured with cardiomyocytes and subjected to a model of ischemia-reperfusion. Although there was a difference between TRPA1 activation or inhibition in vivo, no experimental group was different to control animals in infarct size, which also applies to animals lacking TRPA1. In vitro, survival probability of cardiomyocytes challenged by ischemia-reperfusion increased from 32.8% in absence to 45.1% in presence of sensory neurons, which depends, at least partly, on TRPA1. This study raises doubts about whether TRPA1 is a promising target to reduce myocardial damage within a 24 h period. The results are incompatible with relevant enlargements of infarcts by TRPA1 activation or inhibition, which argues against adverse effects when TRPA1 is targeted for other indications.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms24032516