Late Breaking Abstract - Contribution of STIM-activated TRPC-ORAI channels to the intermittent hypoxia-induced pulmonary hypertension

Castillo-Galán, Sebastián; Arenas, German A.; Krause, Bernardo J.; Iturriaga, Rodrigo

doi:10.1183/13993003.congress-2020.594

Cited by 1 publication

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“…In an experimental obstructive sleep apnea model induced in rats by chronic intermittent hypoxia (CIH) (5% inspired O 2 for 20 s, followed by 280 s of room air, 12 times per hour for 8 h a day for 14 to 28 days), Castillo-Galán et al showed the increased protein expression of Orai1, STIM1, and TRPC1, -C4, -C6 in the lungs of CIH rats [ 180 ]. Treatment of these rats with 2-APB decreased right ventricular systolic pressure (RVSP) and pulmonary vessel remodeling, which increased following CIH exposure [ 181 ].…”

Section: Soce In Pahmentioning

confidence: 99%

Role of Store-Operated Ca2+ Entry in the Pulmonary Vascular Remodeling Occurring in Pulmonary Arterial Hypertension

et al. 2021

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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 Ca2+ homoeostasis could partly explain PASMC dysfunction. One of the most crucial actors regulating Ca2+ homeostasis is store-operated Ca2+ channels, which mediate store-operated Ca2+ 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.

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Section: Soce In Pahmentioning

confidence: 99%