The Pathological Role of Transient Receptor Potential Channels in Heart Disease
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- Watanabe Hiroyuki
- Second Department of Internal Medicine, Akita University School of Medicine
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- Murakami Manabu
- Department of Physiology, Akita University School of Medicine
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- Ohba Takayoshi
- Department of Physiology, Akita University School of Medicine
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- Ono Kyoichi
- Department of Physiology, Akita University School of Medicine
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- Ito Hiroshi
- Second Department of Internal Medicine, Akita University School of Medicine
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Abstract
Transient receptor potential (TRP) channels are expressed in almost every human tissue, including the heart and vasculature. Most are permeable to Ca2+ and play unique roles as multifunctional cellular sensors. Their involvement in many fundamental cell functions (eg, contraction, proliferation, and cell death) has made investigating their roles in human disease an urgent priority for medical science. This review presents an overview of current knowledge about the pathological role of TRP channels in heart disease and highlights some TRP channels with anticipated roles in disease. Evidence suggests that (a) upregulation of TRPC channels is involved in the development of cardiac hypertrophy and heart failure; (b) TRPC1, TRPC6, and TRPV2 play a role in the pathogenesis of cardiomyopathy associated with muscular dystrophy; (c) TRPC6 or TRPM4 is involved in the delayed after-depolarization; (d) TRPP2 is involved in the normal development of the interventricular and interatrial septa; and (e) neuronal TRPV1 acts as a detector of pain-producing stimuli. Ultimately, TRP channels might become novel pharmacological targets in the treatment of human heart disease. (Circ J 2009; 73: 419 - 427)<br>
Journal
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- Circulation Journal
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Circulation Journal 73 (3), 419-427, 2009
The Japanese Circulation Society
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Details 詳細情報について
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- CRID
- 1390282680079585408
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- NII Article ID
- 110007126743
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- NII Book ID
- AA11591968
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- ISSN
- 13474820
- 13469843
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- Text Lang
- en
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- Data Source
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- JaLC
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed