Transient Receptor Potential Ankyrin 1 Activation within the Cardiac Myocyte Limits Ischemia–reperfusion Injury in Rodents

Lu, Yao; Piplani, Honit; McAllister, Stacy L.; Hurt, Carl M.; Gross, Eric R.

doi:10.1097/aln.0000000000001377

Cited by 34 publications

(28 citation statements)

References 35 publications

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“…In relation to the expression and function of other TRP channels in heart, TRPA1 was detected in cardiac endothelial cells, vascular smooth muscle, and in cardiac myocytes (Yue et al., 2015), where its activation seems relevant to attenuate ischemia and reperfusion injury (Lu et al., 2016). Furthermore, the presence of TRPP2 has been proven in knockout mice who died before birth as a result of cardiac malformations (Pennekamp et al., 2002).…”

Section: Expression Of Trp Channels In Cardiac Cellsmentioning

confidence: 99%

TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling

et al. 2019

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Calcium is an important second messenger required not only for the excitation-contraction coupling of the heart but also critical for the activation of cell signaling pathways involved in the adverse cardiac remodeling and consequently for the heart failure. Sustained neurohumoral activation, pressure-overload, or myocardial injury can cause pathologic hypertrophic growth of the heart followed by interstitial fibrosis. The consequent heart’s structural and molecular adaptation might elevate the risk of developing heart failure and malignant arrhythmia. Compelling evidences have demonstrated that Ca 2+ entry through TRP channels might play pivotal roles in cardiac function and pathology. TRP proteins are classified into six subfamilies: TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPA (ankyrin), TRPML (mucolipin), and TRPP (polycystin), which are activated by numerous physical and/or chemical stimuli. TRP channels participate to the handling of the intracellular Ca 2+ concentration in cardiac myocytes and are mediators of different cardiovascular alterations. This review provides an overview of the current knowledge of TRP proteins implication in the pathologic process of some frequent cardiac diseases associated with the adverse cardiac remodeling such as cardiac hypertrophy, fibrosis, and conduction alteration.

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Section: Expression Of Trp Channels In Cardiac Cellsmentioning

confidence: 99%

TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling

et al. 2019

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“…Accumulating evidence indicates the important role of TRPA1 in the pathophysiology of cardiac disease [ 10 ]. TRPA1 activators given prophylactically could reduce the infarct size in a rat model of myocardial ischemia-reperfusion injury [ 11 ]. However, the role of TRPA1 in Dox-induced cardiotoxicity is still unknown.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of TRPA1 Attenuates Doxorubicin‐Induced Acute Cardiotoxicity by Suppressing Oxidative Stress, the Inflammatory Response, and Endoplasmic Reticulum Stress

Wang

Liu

et al. 2018

Oxidative Medicine and Cellular Longevity

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The transient receptor potential ankyrin 1 (TRPA1) channel is expressed in cardiomyocytes and involved in many cardiovascular diseases. However, the expression and function of TRPA1 in doxorubicin- (Dox-) induced acute cardiotoxicity have not been elucidated. This study aimed at investigating whether blocking the TRPA1 channel with the specific inhibitor HC-030031 (HC) attenuates Dox-induced cardiac injury. The animals were randomly divided into four groups: control, HC, Dox, and Dox + HC. Echocardiography was used to evaluate cardiac function, and the heart was removed for molecular experiments. The results showed that the expression of TRPA1 was increased in the heart after Dox treatment. Cardiac dysfunction and increased serum CK-MB and LDH levels were induced by Dox, but these effects were attenuated by HC treatment. In addition, HC mitigated Dox-induced oxidative stress, as evidenced by the decreased MDA level and increased GSH level and SOD activity in the Dox + HC group. Meanwhile, HC treatment lowered the levels of the proinflammatory cytokines IL-1β, IL-6, IL-17, and TNF-α induced by Dox. Furthermore, HC treatment mitigated endoplasmic reticulum (ER) stress and cardiomyocyte apoptosis induced by Dox. These results indicated that inhibition of TRPA1 could prevent Dox-induced cardiomyocyte apoptosis in mice by inhibiting oxidative stress, inflammation, and ER stress.

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“…Oxidation and peroxidation of cysteine residues cause residues to bind to disulfide bonds, which enhances TRPA1 activity ( MacPherson et al, 2007a ). TRPA1 is present in cardiomyocytes and is important in regulating myocardial reperfusion injury ( Lu et al, 2016 ). A study showed that TRPA1 gene-knockout myocardial ischemia–reperfusion mice alleviated myocardial injury, indicating that TRPA1 channel activation mediates myocardial ischemia–reperfusion injury ( Conklin et al, 2019 ).…”

Section: Trpa1 and Common Cardiovascular Diseasesmentioning

confidence: 99%

Transient Receptor Potential Ankyrin Type-1 Channels as a Potential Target for the Treatment of Cardiovascular Diseases

et al. 2020

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Cardiovascular disease is one of the chronic conditions with the highest mortality rate in the world. Underlying conditions such as hypertension, metabolic disorders, and habits like smoking are contributors to the manifestation of cardiovascular diseases. The treatment of cardiovascular diseases is inseparable from the development of drugs. Consequently, this has led to many researchers to focus on the search for effective drug targets. The transient receptor potential channel Ankyrin 1 (TRPA1) subtype is a non-selective cation channel, which belongs to the transient receptor potential (TRP) ion channel. Previous studies have shown that members of the TRP family contribute significantly to cardiovascular disease. However, many researchers have not explored the role of TRPA1 as a potential target for the treatment of cardiovascular diseases. Furthermore, recent studies revealed that TRPA1 is commonly expressed in the vascular endothelium. The endothelium is linked to the causes of some cardiovascular diseases, such as atherosclerosis, myocardial fibrosis, heart failure, and arrhythmia. The activation of TRPA1 has a positive effect on atherosclerosis, but it has a negative effect on other cardiovascular diseases such as myocardial fibrosis and heart failure. This review introduces the structural and functional characteristics of TRPA1 and its importance on vascular physiology and common cardiovascular diseases. Moreover, this review summarizes some evidence that TRPA1 is correlated to cardiovascular disease risk factors.

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Transient Receptor Potential Ankyrin 1 Activation within the Cardiac Myocyte Limits Ischemia–reperfusion Injury in Rodents

Cited by 34 publications

References 35 publications

TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling

TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling

Inhibition of TRPA1 Attenuates Doxorubicin‐Induced Acute Cardiotoxicity by Suppressing Oxidative Stress, the Inflammatory Response, and Endoplasmic Reticulum Stress

Transient Receptor Potential Ankyrin Type-1 Channels as a Potential Target for the Treatment of Cardiovascular Diseases

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