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. 2020 Mar 23;33:101516. doi: 10.1016/j.redox.2020.101516

Table 1.

Implications of ER oxidoreductases and/or ER stress in lung fibrosis or extracellular matrix biology.

ER oxidoreductase Putative function Model References
PDIA3 Fas-SS formation, Epithelial cell apoptosis
AEC2- AEC1 differentiation, regulation of Wnt/β-catenin signaling
Epithelial cells,
Mouse models, IPF
Primary lung epithelial cells
[87]
[93]
PDI Disulfide bond formation in LOXL2, collagen 1a1, transglutaminase 2, matrix metalloproteinase 9,
Non-catalytic component of prolyl-4 hydroxylase
Integrin mediated adhesion
Cell lines, mouse models
Human renal fibrosis
Rat liver, chick embryos, C. Elegans
Platelets
[75,[95], [96], [97]]
[100,101]
[98]
ERO1α, ERO1β PRDX4 Prolyl-4 hydroxylation of collagen Triple knock out mice
Mouse embryonic fibroblasts
[111]
PRDX4 Protection of NASH and diabetes Mouse model [117]
TXNDC5 Stabilization of ECM proteins,
Augmentation of cardiac fibrosis
Cardiac fibroblasts, mice [112]
QSOX1 Laminin incorporation in the ECM mice, fibroblasts [113]
GPX7 Regulation for longevity, protection from senescence Mouse models
Fibroblasts, mesenchymal stem cells
C.Elegans
[116]
Fibronectin Intrinsic PDI activity In vitro [99]
VKOR Promotes cisplatin-induced hepatic fibrosis rats [114]