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Elevated ROS levels disrupt cellular organelles, induce stress response pathways, and activate apoptosis and fibrotic signaling, collectively impeding effective tendon healing ( FIGURE 1 Understanding the sources and regulation of ROS in tendons, including the roles of nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, mitochondria, and the hypoxia-inducible factor (HIF), is crucial for distinguishing between their beneficial and harmful effects

2021;320:G52130

The primary therapeutic objective during this phase is timely reperfusion-achieved through thrombolysis or mechanical thrombectomy-to restore cerebral blood flow and limit infarct expansion

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