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New insights into targeting mitochondria in ischemic injury
- Source :
- Apoptosis. 26:163-183
- Publication Year :
- 2021
- Publisher :
- Springer Science and Business Media LLC, 2021.
-
Abstract
- Stroke is the leading cause of adult disability and death worldwide. Mitochondrial dysfunction has been recognized as a marker of neuronal death during ischemic stroke. Maintaining the function of mitochondria is important for improving the survival of neurons and maintaining neuronal function. Damaged mitochondria induce neuronal cell apoptosis by releasing reactive oxygen species (ROS) and pro-apoptotic factors. Mitochondrial fission and fusion processes and mitophagy are of great importance to mitochondrial quality control. This paper reviews the dynamic changes in mitochondria, the roles of mitochondria in different cell types, and related signaling pathways in ischemic stroke. This review describes in detail the role of mitochondria in the process of neuronal injury and protection in cerebral ischemia, and integrates neuroprotective drugs targeting mitochondria in recent years, which may provide a theoretical basis for the progress of treatment of ischemic stroke. The potential of mitochondrial-targeted therapy is also emphasized, which provides valuable insights for clinical research.
- Subjects :
- 0301 basic medicine
Cancer Research
Clinical Biochemistry
Ischemia
Pharmaceutical Science
Apoptosis
Mitochondrion
Mitochondrial Dynamics
Brain Ischemia
03 medical and health sciences
Drug Delivery Systems
0302 clinical medicine
Mitophagy
medicine
Animals
Humans
Stroke
Neurons
Pharmacology
chemistry.chemical_classification
Reactive oxygen species
business.industry
Biochemistry (medical)
Cell Biology
medicine.disease
Mitochondria
Neuroprotective Agents
030104 developmental biology
chemistry
030220 oncology & carcinogenesis
Mitochondrial fission
Signal transduction
Reactive Oxygen Species
business
Neuroscience
Signal Transduction
Subjects
Details
- ISSN :
- 1573675X and 13608185
- Volume :
- 26
- Database :
- OpenAIRE
- Journal :
- Apoptosis
- Accession number :
- edsair.doi.dedup.....660d1f1209f67a8e04112a3624109a7d