Ischemic stroke is one of the leading causes of disability and death in the world. Elucidation of the underlying mechanisms associated with neuronal death during this detrimental process has been of significant interest in the field of research. One principle component vital to the maintenance of cellular integrity is the cytoskeleton. Studies suggest that abnormalities at the level of this fundamental structure are directly linked to adverse effects on cellular well-being, including cell death. In recent years, evidence has also emerged regarding an imperative role for the transient receptor potential (TRP) family member TRPM7 in the mediation of excitotoxic-independent neuronal demise. In this review, we will elaborate on the current knowledge and unique properties associated with the functioning of this structure. In addition, we will deliberate the involvement of distinct mechanistic pathways during TRPM7-dependent cell death, including modifications at the level of the cytoskeleton.
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