Table 1.

Mechanisms of the Nrf2/HO-1 signaling axis in pediatric respiratory diseases.

Pediatric respiratory disease	Effects	Reference
Pneumonia	Reduces the migration of polymorphonuclear leukocytes in the lung through adenosine receptors 2A and 2B	[42]
	Inhibits ROS production and decreases the expression of inflammatory mediators IL-1β and TNF-α	[43]
	Reduces the migration of CXCL1-related polymorphonuclear white blood cells to the alveolar septum	[44]
Asthma	Regulates antioxidant genes	[46]
	Suppresses ROS and TH17 cells	[48]
	Downregulates serum levels of IgE, IL-4, IL-5, IFN-γ, and IL-13	[50]
Lung neoplasm	Promotes resistance to apoptosis induction	[52]
	Retards malignant lung cancer cell transformation	[53]
	Induces alkaliptosis and ferroptosis	[40, 41]
Acute respiratory distress syndrome	Releases a large number of anti-inflammatory cytokines	[56]
	Improves the barrier function of capillary endothelial cells and reduces capillary permeability	[57]
	Is a probable biomarker of ARDS severity	[59]
Idiopathic pulmonary fibrosis	Inhibits the degree of oxidant stress	[60]
	Decreases the upregulated effects of cell death and apoptosis, expression of fibrosis-related factors, and transformation of fibroblasts to myofibroblasts	[61]
Chronic obstructive pulmonary diseases	Regulates the Th1/Th2 ratio and induces secretion of anti-inflammatory cytokines	[56]
	Affects the expression of antioxidant genes	[63]
	Reduces the burden of oxidation in the lung and reduces apoptosis	[53]