Redox Regulation and Mitochondrial Neuroprotection in Ischemic Stroke: The Emerging Role of DJ ‐1 ( PARK7 )
Abstract
Ischemic stroke remains a leading cause of global mortality and long-term disability, driven largely by oxidative stress, mitochondrial dysfunction, and inflammatory cascades. DJ-1 (PARK7), a redox-sensitive protein originally implicated in Parkinson's disease, has emerged as a critical neuroprotective regulator in cerebral ischemia. Oxidation of its cysteine-106 residue enables DJ-1 to stabilize mitochondrial function, suppress reactive oxygen species, and activate Nrf2-dependent antioxidant defenses. DJ-1 deficiency markedly exacerbates infarct size and neuronal vulnerability, whereas its activation confers robust neuroprotection. This review highlights DJ-1 as a promising redox-responsive therapeutic target for limiting ischemic brain injury.
Fields of Study & Subjects
Parkinson's Disease Mechanisms and Treatments
Neuroinflammation and Neurodegeneration Mechanisms
Advanced Glycation End Products research
Publication details
- Journal / source
- Comprehensive physiology
- Publisher
- Wiley
- Volume
- 16
- Issue
- 3
- Pages
- e70182–e70182
- Publication date
- 24 May 2026
- Language
- EN