Role of Store-Operated Ca<sup>2+</sup> Entry in the Pulmonary Vascular Remodeling Occurring in Pulmonary Arterial Hypertension
Pulmonary arterial hypertension (PAH) is a severe and multifactorial disease. PAH pathogenesis mostly involves pulmonary arterial endothelial and pulmonary arterial smooth muscle cell (PASMC) dysfunction, leading to alterations in pulmonary arterial tone and distal pulmonary vessel obstruction and r...
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| Format: | Article |
| Language: | English |
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MDPI AG
2021-11-01
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| Series: | Biomolecules |
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| Online Access: | https://www.mdpi.com/2218-273X/11/12/1781 |
| _version_ | 1797506433472790528 |
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| author | Bastien Masson David Montani Marc Humbert Véronique Capuano Fabrice Antigny |
| author_facet | Bastien Masson David Montani Marc Humbert Véronique Capuano Fabrice Antigny |
| author_sort | Bastien Masson |
| collection | DOAJ |
| description | Pulmonary arterial hypertension (PAH) is a severe and multifactorial disease. PAH pathogenesis mostly involves pulmonary arterial endothelial and pulmonary arterial smooth muscle cell (PASMC) dysfunction, leading to alterations in pulmonary arterial tone and distal pulmonary vessel obstruction and remodeling. Unfortunately, current PAH therapies are not curative, and therapeutic approaches mostly target endothelial dysfunction, while PASMC dysfunction is under investigation. In PAH, modifications in intracellular Ca<sup>2+</sup> homoeostasis could partly explain PASMC dysfunction. One of the most crucial actors regulating Ca<sup>2+</sup> homeostasis is store-operated Ca<sup>2+</sup> channels, which mediate store-operated Ca<sup>2+</sup> entry (SOCE). This review focuses on the main actors of SOCE in human and experimental PASMC, their contribution to PAH pathogenesis, and their therapeutic potential in PAH. |
| first_indexed | 2024-03-10T04:32:36Z |
| format | Article |
| id | doaj.art-3a093708f8754170a02b4fef0bf8bc3a |
| institution | Directory Open Access Journal |
| issn | 2218-273X |
| language | English |
| last_indexed | 2024-03-10T04:32:36Z |
| publishDate | 2021-11-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomolecules |
| spelling | doaj.art-3a093708f8754170a02b4fef0bf8bc3a2023-11-23T03:59:02ZengMDPI AGBiomolecules2218-273X2021-11-011112178110.3390/biom11121781Role of Store-Operated Ca<sup>2+</sup> Entry in the Pulmonary Vascular Remodeling Occurring in Pulmonary Arterial HypertensionBastien Masson0David Montani1Marc Humbert2Véronique Capuano3Fabrice Antigny4Faculté de Médecine, School of Medicine, Université Paris-Saclay, 94276 Le Kremlin-Bicêtre, FranceFaculté de Médecine, School of Medicine, Université Paris-Saclay, 94276 Le Kremlin-Bicêtre, FranceFaculté de Médecine, School of Medicine, Université Paris-Saclay, 94276 Le Kremlin-Bicêtre, FranceFaculté de Médecine, School of Medicine, Université Paris-Saclay, 94276 Le Kremlin-Bicêtre, FranceFaculté de Médecine, School of Medicine, Université Paris-Saclay, 94276 Le Kremlin-Bicêtre, FrancePulmonary arterial hypertension (PAH) is a severe and multifactorial disease. PAH pathogenesis mostly involves pulmonary arterial endothelial and pulmonary arterial smooth muscle cell (PASMC) dysfunction, leading to alterations in pulmonary arterial tone and distal pulmonary vessel obstruction and remodeling. Unfortunately, current PAH therapies are not curative, and therapeutic approaches mostly target endothelial dysfunction, while PASMC dysfunction is under investigation. In PAH, modifications in intracellular Ca<sup>2+</sup> homoeostasis could partly explain PASMC dysfunction. One of the most crucial actors regulating Ca<sup>2+</sup> homeostasis is store-operated Ca<sup>2+</sup> channels, which mediate store-operated Ca<sup>2+</sup> entry (SOCE). This review focuses on the main actors of SOCE in human and experimental PASMC, their contribution to PAH pathogenesis, and their therapeutic potential in PAH.https://www.mdpi.com/2218-273X/11/12/1781PAHCa<sup>2+</sup> signalingOraiSTIMTRPCIP<sub>3</sub>R |
| spellingShingle | Bastien Masson David Montani Marc Humbert Véronique Capuano Fabrice Antigny Role of Store-Operated Ca<sup>2+</sup> Entry in the Pulmonary Vascular Remodeling Occurring in Pulmonary Arterial Hypertension Biomolecules PAH Ca<sup>2+</sup> signaling Orai STIM TRPC IP<sub>3</sub>R |
| title | Role of Store-Operated Ca<sup>2+</sup> Entry in the Pulmonary Vascular Remodeling Occurring in Pulmonary Arterial Hypertension |
| title_full | Role of Store-Operated Ca<sup>2+</sup> Entry in the Pulmonary Vascular Remodeling Occurring in Pulmonary Arterial Hypertension |
| title_fullStr | Role of Store-Operated Ca<sup>2+</sup> Entry in the Pulmonary Vascular Remodeling Occurring in Pulmonary Arterial Hypertension |
| title_full_unstemmed | Role of Store-Operated Ca<sup>2+</sup> Entry in the Pulmonary Vascular Remodeling Occurring in Pulmonary Arterial Hypertension |
| title_short | Role of Store-Operated Ca<sup>2+</sup> Entry in the Pulmonary Vascular Remodeling Occurring in Pulmonary Arterial Hypertension |
| title_sort | role of store operated ca sup 2 sup entry in the pulmonary vascular remodeling occurring in pulmonary arterial hypertension |
| topic | PAH Ca<sup>2+</sup> signaling Orai STIM TRPC IP<sub>3</sub>R |
| url | https://www.mdpi.com/2218-273X/11/12/1781 |
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