Mitochondria in Cell-Based Therapy for Stroke.
Molly MonsourJonah GordonGavin Miles LockardAdam AlayliCesario Venturina BorlonganPublished in: Antioxidants (Basel, Switzerland) (2023)
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.
Keyphrases
- cell death
- stem cells
- atrial fibrillation
- cerebral ischemia
- cell therapy
- single cell
- traumatic brain injury
- oxidative stress
- cell cycle arrest
- acute myocardial infarction
- reactive oxygen species
- heart failure
- subarachnoid hemorrhage
- coronary artery disease
- endoplasmic reticulum
- cell proliferation
- signaling pathway
- acute coronary syndrome
- brain injury
- lipopolysaccharide induced
- ischemia reperfusion injury
- bone marrow