Table 1.

Mechanism of ROS damage in specific complications.

Pulmonary hypertension (PHT)	Chronic hypoxia-vascular remodeling with medial hypertrophy due to NADPH oxidases
Delayed wound healing	(i) ROS/reactive nitrogen species (RNS) overproduction prolongs the inflammation in chronic wounds as both ROS and RNS stimulate neutrophil and macrophage chemotaxis and migration (ii) Direct cellular effects of ROS/RNS include impaired migratory, proliferative and extracellular matrix (ECM) synthetic properties of dermal fibroblasts, and keratinocytes
Thrombosis	(i) Propagation of platelet activation by inactivating nitric oxide (ii) Release of platelet agonists such as ADP, giving formation of isoprostanes and ox-LDL causing the release of proatherogenic molecules such as CD40L which are mainly produced by NADPH oxidase
Osteoporosis	NOX1, NOX2, and NOX4 (NOX family of NADPH oxidases) play role in bone resorption due to activation of mature osteoclasts
Silent brain infarcts	NOX2 imbalance causes brain injury/stroke