Publications by authors named "Mona Ruban"
Background And Purpose: Fibrotic lung remodelling after a respiratory viral infection represents a debilitating clinical sequela. Studying or managing viral-fibrotic sequela remains challenging, due to limited therapeutic options and lack of understanding of mechanisms. This study determined whether protein disulfide isomerase A3 (PDIA3) and secreted phosphoprotein 1 (SPP1), which are associated with pulmonary fibrosis, can promote influenza-induced lung fibrotic remodelling and whether inhibition of PDIA3 or SPP1 can resolve viral-mediated fibrotic remodelling.
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- - Influenza neuraminidase (NA) is crucial for the virus to exit infected cells, and its function relies on disulfide bonds, which may be facilitated by protein disulfide isomerase (PDI)A3.
- - Researchers investigated the role of PDIA3 in the maturation and activity of NA using various assays, discovering that the interaction between NA and PDIA3 is essential for NA activity and overall viral propagation.
- - The use of a PDI-specific inhibitor (LOC14) in mouse models showed reduced NA activity and viral burden, suggesting that targeting PDIA3 could be a new strategy for developing antiviral treatments against influenza.
Background: The role of club cells in the pathology of idiopathic pulmonary fibrosis (IPF) is not well understood. Protein disulfide isomerase A3 (PDIA3), an endoplasmic reticulum-based redox chaperone required for the functions of various fibrosis-related proteins; however, the mechanisms of action of PDIA3 in pulmonary fibrosis are not fully elucidated.
Objectives: To examine the role of club cells and PDIA3 in the pathology of pulmonary fibrosis and the therapeutic potential of inhibition of PDIA3 in lung fibrosis.