Mitochondria in Cell-Based Therapy for Stroke

Despite a relatively developed understanding of the pathophysiology underlying primary and secondary mechanisms of cell death after ischemic injury, there are few established treatments to improve stroke prognoses. A major contributor to secondary cell death is mitochondrial dysfunction. Recent advancements in cell-based therapies suggest that stem cells may be revolutionary for treating stroke, and the reestablishment of mitochondrial integrity may underlie these therapeutic benefits. In fact, functioning mitochondria are imperative for reducing oxidative damage and neuroinflammation following stroke and reperfusion injury. In this review, we will discuss the role of mitochondria in establishing the anti-oxidative effects of stem cell therapies for stroke.

Automated summary

Despite a good understanding of the pathophysiology of cell death after ischemic injury, there are few established treatments for stroke. Mitochondrial dysfunction plays a key role in secondary cell death, and recent advancements in stem cell therapies suggest that restoring mitochondrial integrity may be beneficial. This review discusses the role of mitochondria in the anti-oxidative effects of stem cell therapies for stroke.