Circadian rhythm is a master process observed in nearly every type of cell throughout the body, and it macroscopically regulates daily physiology. Recent clinical trials have revealed the effects of circadian variation on the incidence, pathophysiological processes, and prognosis of acute ischemic stroke. Furthermore, core clock genes, the cell-autonomous pacemakers of the circadian rhythm, affect the neurovascular unit-composing cells in a nonparallel manner after the same pathophysiological processes of ischemia/reperfusion. In this review, we discuss the influence of circadian rhythms and clock genes on each type of neurovascular unit cell in the pathophysiological processes of acute ischemic stroke.
Keyphrases
- acute ischemic stroke
- single cell
- clinical trial
- atrial fibrillation
- cell therapy
- heart rate
- genome wide
- induced apoptosis
- randomized controlled trial
- gene expression
- white matter
- oxidative stress
- mesenchymal stem cells
- functional connectivity
- multiple sclerosis
- resting state
- bone marrow
- open label
- cell cycle arrest
- study protocol
- phase ii
- endoplasmic reticulum stress
- bioinformatics analysis