Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

TRPMs and neuronal cell death.

Michelle M Aarts1, Michael Tymianski

  • 1Applied and Interventional Research and Division of Neurosurgery, Toronto Western Research Institute, W4-325, 399 Bathurst Street, Toronto, ON M5T 2S8, Canada.

Pflugers Archiv : European Journal of Physiology
|July 27, 2005
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Sex differences in brain frailty measures and outcomes after endovascular thrombectomy: ESCAPE-NA1 analysis.

Journal of the neurological sciences·2026
Same author

Safety and Efficacy of Nerinetide at Year 1 in Participants Enrolled in ESCAPE-NEXT: A Multicenter, Double-Blind, Randomized Controlled Trial.

Journal of the American Heart Association·2026
Same author

Minimal Sufficient Balance Randomization and Site-Specific Treatment Allocation Imbalance in Multicenter Acute Stroke Trials.

Stroke·2026
Same author

MRI measurement of the delayed secondary ischaemic injury following endovascular thrombectomy: results from the REPERFUSE-NA1 study.

European stroke journal·2026
Same author

Nerinetide Reduces Early Infarct Growth Among Stroke Patients Undergoing EVT Without Intravenous Alteplase.

Stroke (Hoboken, N.J.)·2026
Same author

Evaluating Outcome Prediction Models in Endovascular Stroke Treatment Using Baseline, Treatment, and Posttreatment Variables.

Stroke (Hoboken, N.J.)·2026

New research identifies Transient Receptor Potential Melastatin (TRPM) channels, like TRPM7 and TRPM2, as key players in brain injury-induced neuronal death. This discovery opens new avenues for neuroprotective therapies targeting oxidative stress pathways.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Acute central nervous system (CNS) injury involves complex cell death pathways including excitotoxicity, apoptosis, and inflammation.
  • Previous neuroprotective strategies targeting glutamate receptors, antioxidants, or anti-inflammatories have shown limited clinical success due to issues like narrow therapeutic windows and essential signaling interference.

Purpose of the Study:

  • To explore novel molecular targets for neuroprotection in acute CNS injury.
  • To investigate the role of Transient Receptor Potential (TRP) channels in neuronal death pathways.

Main Methods:

  • Review of recent advances in neuronal biochemistry, genomics, and proteomics.
  • Focus on the expression and function of TRP channels, particularly the melastatin subfamily (TRPM), in the brain.

Related Experiment Videos

  • Analysis of TRPM channel involvement in oxidative stress-induced neuronal death and excitotoxic signaling.

    • Main Results:

    • Transient Receptor Potential (TRP) channels are highly expressed in the brain and some members are induced by oxidative stress.
    • TRP melastatin (TRPM) channel members, specifically TRPM7 and TRPM2, are implicated in neuronal death.
    • These channels appear to mediate cell death activated by oxidative stress and downstream of excitotoxic pathways.

    Conclusions:

    • TRPM7 and TRPM2 channels represent a promising new target for therapeutic intervention in acute neurodegeneration.
    • Understanding the role of TRP channels in oxidative stress and excitotoxicity pathways offers a novel approach to treating brain damage.