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Int J Physiol Pathophysiol Pharmacol 2010;2(2):95-103
Review Article
TRPM2, calcium and neurodegenerative diseases
Yu-Feng Xie, John F. MacDonald, Michael F. Jackson
Robarts Research Institute, Department of Physiology and Pharmacology, Department of Anatomy and Cell biology, University of
Western Ontario, London, Ontario.
Received March 2, 2010, accepted March 8, 2010, available online March 15, 2010
Abstract: NMDA receptor overactivation triggers intracellular Ca2+ 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 Ca2+ influx pathways. Recent studies indicate that TRPM2, a member of the TPRM subfamily of
Ca2+-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 oligomers 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. (IJPPP1003001).
Key words: TRPM2, oxidative stress, neurodegeneration, amyloid beta, stroke, NMDA receptor
Full Text PDF
Address all correspondence to:
Dr. Michael F. Jackson
Robarts Research Institute
University of Western Ontario
100 Perth Drive
London, Ontario N6A 5K8
E-mail: mjackson@robarts.ca
Dr. John F. MacDonald
Robarts Research Institute
University of Western Ontario
100 Perth Drive
London, Ontario N6A 5K8
E-mail: jfmacdonald@robarts.ca
Review Article
TRPM2, calcium and neurodegenerative diseases
Yu-Feng Xie, John F. MacDonald, Michael F. Jackson
Robarts Research Institute, Department of Physiology and Pharmacology, Department of Anatomy and Cell biology, University of
Western Ontario, London, Ontario.
Received March 2, 2010, accepted March 8, 2010, available online March 15, 2010
Abstract: NMDA receptor overactivation triggers intracellular Ca2+ 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 Ca2+ influx pathways. Recent studies indicate that TRPM2, a member of the TPRM subfamily of
Ca2+-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 oligomers 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. (IJPPP1003001).
Key words: TRPM2, oxidative stress, neurodegeneration, amyloid beta, stroke, NMDA receptor
Full Text PDF
Address all correspondence to:
Dr. Michael F. Jackson
Robarts Research Institute
University of Western Ontario
100 Perth Drive
London, Ontario N6A 5K8
E-mail: mjackson@robarts.ca
Dr. John F. MacDonald
Robarts Research Institute
University of Western Ontario
100 Perth Drive
London, Ontario N6A 5K8
E-mail: jfmacdonald@robarts.ca
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