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Review
. 2021 Aug;22(2):881.
doi: 10.3892/etm.2021.10313. Epub 2021 Jun 15.

Advancement in research on the role of the transient receptor potential vanilloid channel in cerebral ischemic injury (Review)

Qian Xie  1 , Rong Ma  1 , Hongyan Li  1 , Jian Wang  1 , Xiaoqing Guo  1 , Hai Chen  1
Affiliations
Review

Advancement in research on the role of the transient receptor potential vanilloid channel in cerebral ischemic injury (Review)

Qian Xie et al. Exp Ther Med. 2021 Aug.

Abstract

Stroke is a common critical disease occurring in middle-aged and elderly individuals, and is characterized by high morbidity, lethality and mortality. As such, it is of great concern to medical professionals. The aim of the present review was to investigate the effects of transient receptor potential vanilloid (TRPV) subtypes during cerebral ischemia in ischemia-reperfusion animal models, oxygen glucose deprivation and in other administration cell models in vitro to explore new avenues for stroke research and clinical treatments. TRPV1, TRPV2 and TRPV4 employ different methodologies by which they confer protection against cerebral ischemic injury. TRPV1 and TRPV4 are likely related to the inhibition of inflammatory reactions, neurotoxicity and cell apoptosis, thus promoting nerve growth and regulation of intracellular calcium ions (Ca2+). The mechanisms of neuroprotection of TRPV1 are the JNK pathway, N-methyl-D-aspartate (NMDA) receptor and therapeutic hypothermia. The mechanisms of neuroprotection of TRPV4 are the PI3K/Akt pathways, NMDA receptor and p38 MAPK pathway, amongst others. The mechanisms by which TRPV2 confers its protective effects are predominantly connected with the regulation of nerve growth factor, MAPK and JNK pathways, as well as JNK-dependent pathways. Thus, TRPVs have the potential for improving outcomes associated with cerebral ischemic or reperfusion injuries. The protection conferred by TRPV1 and TRPV4 is closely related to cellular Ca2+ influx, while TRPV2 has a different target and mode of action, possibly due to its expression sites. However, in light of certain contradictory research conclusions, further experimentation is required to clarify the mechanisms and specific pathways by which TRPVs act to alleviate nerve injuries.

Keywords: cerebral ischemic injury; ischemic stroke; research progress; transient receptor potential vanilloid.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
Associations among the TRPV1, TRPV2 and TRPV4 channels in regard to cerebral ischemia injuries. TRPV, transient receptor potential vanilloid; MEKK, MAP kinase kinase kinase; MKK, mitogen-activated protein kinase kinase; PIP3, phosphatidylinositol (3-5)-trisphosphate; eNOS, endothelial nitric oxide synthase; NO, nitric oxide; NGF, nerve growth factor.
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Grants and funding

Funding: The present study was supported by the National Natural Science Foundation of China (grant nos. 81873023 and 81473371), the Innovation Team in Chengdu University of Traditional Chinese Medicine (grant no. CXTD2018004) and the Open Research Fund of the Key Laboratory of Southwestern Characteristic Chinese Medicine Resources, Chengdu University of Traditional Chinese Medicine (grant no. 2020XSGG025).