scholarly journals Activation of transient receptor potential vanilloid 4 exacerbates myocardial ischemia-reperfusion injury via JNK-CaMKII phosphorylation pathway in isolated mice hearts

Cell Calcium ◽  
2021 ◽  
pp. 102483
Author(s):  
Shaoshao Zhang ◽  
Kai Lu ◽  
Shuaitao Yang ◽  
Yuwei Wu ◽  
Jie Liao ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Transient Receptor Potential ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Transient Receptor ◽  
Myocardial Ischemia Reperfusion

scholarly journals Blockade of Transient Receptor Potential Vanilloid 4 Enhances Antioxidation after Myocardial Ischemia/Reperfusion

2019 ◽  
Vol 2019 ◽  
pp. 1-17 ◽  
Author(s):  
Qiongfeng Wu ◽  
Kai Lu ◽  
Zhaoyang Zhao ◽  
Binbin Wang ◽  
Huixia Liu ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Transient Receptor Potential ◽  
Ischemia Reperfusion ◽  
Receptor Potential ◽  
Nuclear Accumulation ◽  
Transient Receptor Potential Vanilloid ◽  
Antioxidative Stress ◽  
Transient Receptor ◽  
Myocardial Ischemia Reperfusion

Antioxidative stress provides a cardioprotective effect during myocardial ischemia/reperfusion (I/R). Previous research has demonstrated that the blockade of transient receptor potential vanilloid 4 (TRPV4) attenuates myocardial I/R injury. However, the underlying mechanism remains unclear. The current study is aimed at investigating the antioxidative activity of TRPV4 inhibition and elucidating the underlying mechanisms in vitro and ex vivo. We found that the inhibiting TRPV4 by the selective TRPV4 blocker HC-067047 or specific TRPV4-siRNA significantly reduces reactive oxygen species (ROS) and methane dicarboxylic aldehyde (MDA) levels in H9C2 cells exposed to hypoxia/reoxygenation (H/R). Meanwhile, the activity of antioxidative enzymes, particularly superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), is enhanced. Furthermore, after H/R, HC-067047 treatment increases the expression of P-Akt and the translocation of nuclear factor E2-related factor 2 (Nrf2) and related antioxidant response element (ARE) mainly including SOD, GSH-Px, and catalase (CAT). LY294002, an Akt inhibitor, suppresses HC-067047 and specific TRPV4-siRNA-induced Nrf2 expression and its nuclear accumulation. Nrf2 siRNA attenuates HC-067047 and specific TRPV4-siRNA-induced ARE expression. In addition, treatment with LY294002 or Nrf2 siRNA significantly attenuates the antioxidant and anti-injury effects of HC-067047 in vitro. Finally, in experiments on isolated rat hearts, we confirmed the antioxidative stress roles of TRPV4 inhibition during myocardial I/R and the application of exogenous H2O2. In conclusion, the inhibition of TRPV4 exerts cardioprotective effects through enhancing antioxidative enzyme activity and expressions via the Akt/Nrf2/ARE pathway.

A Review on Potential Involvement of TRPV1 Channels in Ischemia–Reperfusion Injury

2017 ◽  
Vol 23 (1) ◽  
pp. 38-45 ◽  
Author(s):  
Puneet Kaur Randhawa ◽  
Amteshwar Singh Jaggi
Keyword(s):  
Reperfusion Injury ◽  
Inflammatory Cytokines ◽  
Transient Receptor Potential ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Receptor Potential ◽  
Transient Receptor Potential Vanilloid ◽  
Channel Activation ◽  
Trpv1 Channels ◽  
Transient Receptor

Besides functioning as thermosensors, transient receptor potential vanilloid 1 (TRPV1) channels play a pivotal role in ischemia–reperfusion injury. Transient receptor potential vanilloid 1 channel activation attenuates ischemia–reperfusion-induced injury in various organs including the heart, lungs, kidneys, and the brain. Transient receptor potential vanilloid 1 channels are expressed on the sensory neurons innervating the myocardium, ventricles of the heart, epicardial surface of the heart, endothelial cells, and the vascular smooth muscle cells. During ischemic conditions, activation of TRPV1 channels on the perivascular nerves stimulates the release of calcitonin gene-related peptide and substance P to produce cardioprotection. Furthermore, TRPV1 channel activation reduces the generation of free radicals and inflammatory cytokines, inhibits neutrophil infiltration, and enhances the production of anti-inflammatory cytokines to reduce ischemia–reperfusion-induced tissue injury. The present review describes the potential involvement of TRPV1 channels and the signaling cascade in attenuating ischemia–reperfusion injury in various organs.

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