Increased susceptibility of aging gastric mucosa to injury and delayed healing: Clinical implications

Figure 1 Actions of aspirin in gastrointestinal tissues. Aspirin low dose has an anti-thrombotic effect on platelets - it mainly inhibits cyclooxygenase (COX)-1 enzyme resulting in inhibition of thromboxane A₂ formation, and impairment of platelet aggregation and their adherence to endothelium, and of thrombi formation. Aspirin induced impaired thrombi formation reduces hemostasis and therefore, increases the risk of gastrointestinal (GI) ulcers and bleeding. Aspirin increases GI mucosal injury and has an anti-angiogenic effect since it inhibits COX-1 and COX-2 enzymes in the GI mucosa and in endothelial cells resulting in the reduction of the cytoprotective prostaglandin E₂ and prostacyclin. This causes impaired mucosal integrity and defense, thus increasing the risk of GI ulcers and bleeding and impaired mucosal healing. GI: Gastrointestinal; COX: Cyclooxygenase; TXA₂: Thromboxane A₂; PGE₂: Prostaglandin E₂; PGI₂: Prostacyclin.