The Role of TRP Channels and PMCA in Brain Disorders: Intracellular Calcium and pH Homeostasis
Brain disorders include neurodegenerative diseases (NDs) with different conditions that primarily affect the neurons and glia in the brain. However, the risk factors and pathophysiological mechanisms of NDs have not been fully elucidated. Homeostasis of intracellular Ca2+ concentration and intracell...
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Frontiers Media S.A.
2021-01-01
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| Series: | Frontiers in Cell and Developmental Biology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fcell.2021.584388/full |
| _version_ | 1818617350580076544 |
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| author | Sung-Min Hwang Ji Yeon Lee Chul-Kyu Park Yong Ho Kim |
| author_facet | Sung-Min Hwang Ji Yeon Lee Chul-Kyu Park Yong Ho Kim |
| author_sort | Sung-Min Hwang |
| collection | DOAJ |
| description | Brain disorders include neurodegenerative diseases (NDs) with different conditions that primarily affect the neurons and glia in the brain. However, the risk factors and pathophysiological mechanisms of NDs have not been fully elucidated. Homeostasis of intracellular Ca2+ concentration and intracellular pH (pHi) is crucial for cell function. The regulatory processes of these ionic mechanisms may be absent or excessive in pathological conditions, leading to a loss of cell death in distinct regions of ND patients. Herein, we review the potential involvement of transient receptor potential (TRP) channels in NDs, where disrupted Ca2+ homeostasis leads to cell death. The capability of TRP channels to restore or excite the cell through Ca2+ regulation depending on the level of plasma membrane Ca2+ ATPase (PMCA) activity is discussed in detail. As PMCA simultaneously affects intracellular Ca2+ regulation as well as pHi, TRP channels and PMCA thus play vital roles in modulating ionic homeostasis in various cell types or specific regions of the brain where the TRP channels and PMCA are expressed. For this reason, the dysfunction of TRP channels and/or PMCA under pathological conditions disrupts neuronal homeostasis due to abnormal Ca2+ and pH levels in the brain, resulting in various NDs. This review addresses the function of TRP channels and PMCA in controlling intracellular Ca2+ and pH, which may provide novel targets for treating NDs. |
| first_indexed | 2024-12-16T17:04:18Z |
| format | Article |
| id | doaj.art-35bd79d43b35475bbda070158285795a |
| institution | Directory Open Access Journal |
| issn | 2296-634X |
| language | English |
| last_indexed | 2024-12-16T17:04:18Z |
| publishDate | 2021-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cell and Developmental Biology |
| spelling | doaj.art-35bd79d43b35475bbda070158285795a2022-12-21T22:23:37ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2021-01-01910.3389/fcell.2021.584388584388The Role of TRP Channels and PMCA in Brain Disorders: Intracellular Calcium and pH HomeostasisSung-Min Hwang0Ji Yeon Lee1Chul-Kyu Park2Yong Ho Kim3Gachon Pain Center, Department of Physiology, Gachon University College of Medicine, Incheon, South KoreaGil Medical Center, Department of Anesthesiology and Pain Medicine, Gachon University, Incheon, South KoreaGachon Pain Center, Department of Physiology, Gachon University College of Medicine, Incheon, South KoreaGachon Pain Center, Department of Physiology, Gachon University College of Medicine, Incheon, South KoreaBrain disorders include neurodegenerative diseases (NDs) with different conditions that primarily affect the neurons and glia in the brain. However, the risk factors and pathophysiological mechanisms of NDs have not been fully elucidated. Homeostasis of intracellular Ca2+ concentration and intracellular pH (pHi) is crucial for cell function. The regulatory processes of these ionic mechanisms may be absent or excessive in pathological conditions, leading to a loss of cell death in distinct regions of ND patients. Herein, we review the potential involvement of transient receptor potential (TRP) channels in NDs, where disrupted Ca2+ homeostasis leads to cell death. The capability of TRP channels to restore or excite the cell through Ca2+ regulation depending on the level of plasma membrane Ca2+ ATPase (PMCA) activity is discussed in detail. As PMCA simultaneously affects intracellular Ca2+ regulation as well as pHi, TRP channels and PMCA thus play vital roles in modulating ionic homeostasis in various cell types or specific regions of the brain where the TRP channels and PMCA are expressed. For this reason, the dysfunction of TRP channels and/or PMCA under pathological conditions disrupts neuronal homeostasis due to abnormal Ca2+ and pH levels in the brain, resulting in various NDs. This review addresses the function of TRP channels and PMCA in controlling intracellular Ca2+ and pH, which may provide novel targets for treating NDs.https://www.frontiersin.org/articles/10.3389/fcell.2021.584388/fullTRP channelsbrain pathologyneurodegenerative diseasescalciumpHhomeostasis |
| spellingShingle | Sung-Min Hwang Ji Yeon Lee Chul-Kyu Park Yong Ho Kim The Role of TRP Channels and PMCA in Brain Disorders: Intracellular Calcium and pH Homeostasis Frontiers in Cell and Developmental Biology TRP channels brain pathology neurodegenerative diseases calcium pH homeostasis |
| title | The Role of TRP Channels and PMCA in Brain Disorders: Intracellular Calcium and pH Homeostasis |
| title_full | The Role of TRP Channels and PMCA in Brain Disorders: Intracellular Calcium and pH Homeostasis |
| title_fullStr | The Role of TRP Channels and PMCA in Brain Disorders: Intracellular Calcium and pH Homeostasis |
| title_full_unstemmed | The Role of TRP Channels and PMCA in Brain Disorders: Intracellular Calcium and pH Homeostasis |
| title_short | The Role of TRP Channels and PMCA in Brain Disorders: Intracellular Calcium and pH Homeostasis |
| title_sort | role of trp channels and pmca in brain disorders intracellular calcium and ph homeostasis |
| topic | TRP channels brain pathology neurodegenerative diseases calcium pH homeostasis |
| url | https://www.frontiersin.org/articles/10.3389/fcell.2021.584388/full |
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