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. 2010 Mar 15;2(2):95-103.

TRPM2, calcium and neurodegenerative diseases

Yu-Feng Xie, John F Macdonald, Michael F Jackson

TRPM2, calcium and neurodegenerative diseases

Yu-Feng Xie et al. Int J Physiol Pathophysiol Pharmacol. .

Abstract

NMDA receptor overactivation triggers intracellular Ca(2+) dysregulation, which has long been thought to be critical for initiating excitotoxic cell death cascades associated with stroke and neurodegenerative disease. The inability of NMDA receptor antagonists to afford neuroprotection in clinical stroke trials has led to a re-evaluation of excitotoxic models of cell death and has focused research efforts towards identifying additional Ca(2+) influx pathways. Recent studies indicate that TRPM2, a member of the TRPM subfamily of Ca(2+)-permeant, non-selective cation channel, plays an important role in mediating cellular responses to a wide range of stimuli that, under certain situations, can induce cell death. These include reactive oxygen and nitrogen species, tumour necrosis factor as well as soluble oli-gomers of amyloid beta. However, the molecular basis of TRPM2 channel involvement in these processes is not fully understood. In this review, we summarize recent studies about the regulation of TRPM2, its interaction with calcium and the possible implications for neurodegenerative diseases.

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Figures

Figure 1
Figure 1
Schematic diagraph showing the signal pathway of TRPM2 and NMDAR. Abbreviations see text.
See this image and copyright information in PMC

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