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Dual Role of TRPV1 Channels in Cerebral Stroke: An Exploration from a Mechanistic and Therapeutic Perspective

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Abstract

Transient receptor potential vanilloid subfamily member 1 (TRPV1) has been strongly implicated in the pathophysiology of cerebral stroke. However, the exact role and mechanism remain elusive. TPRV1 channels are exclusively present in the neurovascular system and involve many neuronal processes. Numerous experimental investigations have demonstrated that TRPV1 channel blockers or the lack of TRPV1 channels may prevent harmful inflammatory responses during ischemia–reperfusion injury, hence conferring neuroprotection. However, TRPV1 agonists such as capsaicin and some other non-specific TRPV1 activators may induce transient/slight degree of TRPV1 channel activation to confer neuroprotection through a variety of mechanisms, including hypothermia induction, improving vascular functions, inducing autophagy, preventing neuronal death, improving memory deficits, and inhibiting inflammation. Another factor in capsaicin-mediated neuroprotection could be the desensitization of TRPV1 channels. Based on the summarized evidence, it may be plausible to suggest that TPRV1 channels have a dual role in ischemia–reperfusion-induced cerebral injury, and thus, both agonists and antagonists may produce neuroprotection depending upon the dose and duration. The current review summarizes the dual function of TRPV1 in ischemia–reperfusion-induced cerebral injury models, explains its mechanism, and predicts the future.

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Abbreviations

BACCO :

Bilateral carotid artery occlusion

BCP :

Beta-caryophyllene

BDNF :

Brain-derived neurotrophic factor

C.B. :

Cannabinoid

DRG :

Dorsal root of ganglia

EA :

Electroacupuncture

E.R. :

Endoplasmic reticulum

ERK :

Extracellular signal-regulated kinase

eNOS :

Endothelial nitric oxide synthase

FAF1 :

Fas-associated factor

ICV :

Intracerebrovascular

JNK :

C-Jun N terminal kinase

MAM :

Mitochondrial-associated membrane

MAPK :

Mitogenic

MCAO :

Middle cerebral artery occlusion

MNF2 :

Mitofusin 2

NF-kB :

Nuclear factor kappa B

NS :

Nitrosative stress

O.S.:

Oxidative stress

ROS :

Reactive oxygen species

SNPC :

Substantia nigra pars compacta

TG :

Trigeminal neurons

TLR :

Toll-like receptor

TrkB :

Tropomyosin receptor kinases B

TRPV1 :

Transient receptor potential vanilloid ion channel one

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Acknowledgements

The authors are thankful to the Central University of Punjab, Bathinda, India, for providing research facilities.

Funding

The authors are thankful to the Ministry of Tribal Affairs, Government of India, for providing NFST financial support. The authors are also grateful to the Department of Science and Technology–Science and Engineering Research Board EEQ/2022/000997, New Delhi, for their gratefulness for providing us financial assistance and Central University of Punjab, Bathinda, India, for supporting us.

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  1. Department of Pharmacology, Central University of Punjab, Bathinda, 151401, India

    Mohd Hanifa, Manisha Suri, Harshita Singh, Riya Gagnani & Anjana Bali

  2. Prosper Pharmacy, 18765, Fraser Highway, Surrey, British Columbia, Canada

    Amteshwar Singh Jaggi

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MH and MS collected the literature and wrote the manuscript. HS reviewed the findings and hypothesized the plausible mechanism. RG finalized the table and figures. ASJ analyzed the manuscript findings and wrote the paper. AB drafted the idea and prepared the manuscript. All authors have contributed equally.

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Correspondence to Amteshwar Singh Jaggi or Anjana Bali.

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Hanifa, M., Suri, M., Singh, H. et al. Dual Role of TRPV1 Channels in Cerebral Stroke: An Exploration from a Mechanistic and Therapeutic Perspective. Mol Neurobiol (2024). https://doi.org/10.1007/s12035-024-04221-5

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