Pituitary Adenylate Cyclase-Activating Polypeptide: A Potent Therapeutic Agent in Oxidative Stress.
Nadia SadanandanBlaise CozeneYou Jeong ParkJeffrey FarooqChase KingsburyZhen-Jie WangAlexa MoscatelloMadeline SaftJustin ChoBella Gonzales-PortilloCesar V BorlonganPublished in: Antioxidants (Basel, Switzerland) (2021)
Stroke is a life-threatening condition that is characterized by secondary cell death processes that occur after the initial disruption of blood flow to the brain. The inability of endogenous repair mechanisms to sufficiently support functional recovery in stroke patients and the inadequate treatment options available are cause for concern. The pathology behind oxidative stress in stroke is of particular interest due to its detrimental effects on the brain. The oxidative stress caused by ischemic stroke overwhelms the neutralization capacity of the body's endogenous antioxidant system, which leads to an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and eventually results in cell death. The overproduction of ROS compromises the functional and structural integrity of brain tissue. Therefore, it is essential to investigate the mechanisms involved in oxidative stress to help obtain adequate treatment options for stroke. Here, we focus on the latest preclinical research that details the mechanisms behind secondary cell death processes that cause many central nervous system (CNS) disorders, as well as research that relates to how the neuroprotective molecular mechanisms of pituitary adenylate cyclase-activating polypeptides (PACAPs) could make these molecules an ideal candidate for the treatment of stroke.
Keyphrases
- cell death
- oxidative stress
- atrial fibrillation
- cerebral ischemia
- dna damage
- reactive oxygen species
- blood flow
- cell cycle arrest
- ischemia reperfusion injury
- diabetic rats
- white matter
- induced apoptosis
- blood brain barrier
- resting state
- signaling pathway
- subarachnoid hemorrhage
- stem cells
- brain injury
- mesenchymal stem cells
- multiple sclerosis
- cell therapy
- cell proliferation
- amino acid