Mitochondrial dysfunction in neurodegenerative diseases and drug targets via apoptotic signaling
| Autor: | Jielong Jiang, Meiqiao Chen, Yuanbo Wu |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Cell signaling Excitotoxicity Apoptosis Disease Mitochondrion medicine.disease_cause Pathogenesis 03 medical and health sciences 0302 clinical medicine medicine Animals Humans Molecular Biology business.industry Multiple sclerosis Neurodegeneration Neurodegenerative Diseases Cell Biology medicine.disease Mitochondria Oxidative Stress 030104 developmental biology Cancer research Molecular Medicine business 030217 neurology & neurosurgery Oxidative stress Signal Transduction |
| Zdroj: | Mitochondrion. 49:35-45 |
| ISSN: | 1567-7249 |
| DOI: | 10.1016/j.mito.2019.07.003 |
| Popis: | Mitochondrial dysfunction is becoming one of the most emerging pathological process in the etiology of neurological disorders. Other common etiologies of the neurological disorders are aging and oxidative stress. Neurodegenerative disorders for instance Huntington's disease, Parkinson's disease, Amyotrophic lateral sclerosis, Epilepsy, Schizophrenia, Multiple sclerosis, Neuropathic pain and Alzheimer's disease involves mitochondrial dysfunction and is regarded as the core of their pathological processes. Most central pathological feature of the neurodegenerative diseases is apoptosis which is regulated by mitochondria. Altered signaling of the apoptotic mechanisms are involved in neurodegeneration. Abnormal levels of these molecular apoptotic proteins promotes the pathogenesis of neurological disorders. Mitochondria are also implicated in the production of reactive oxygen species (ROS). Raised ROS levels initiates the cascade leading to the non-apoptotic death of cells. ROS produced in cells acts as signaling molecules, but when produced in abundance will result in cellular consequences to deoxyribonucleic acid, proteins and lipids, decreased effectiveness of cellular mechanisms, initiation of inflammatory pathways, excitotoxicity, protein agglomeration and apoptosis. Protecting mitochondrial function has been identified as the most effective therapeutic approach to attenuate the pathogenesis of neurodegenerative diseases. This review aims to provide an insight into the mitochondrial dysfunction in the pathogenesis of neurological disorders, alteration in signaling cascades of apoptosis in mitochondrial dysfunction and the therapeutic strategies (both natural and synthetic drugs) targeting these mitochondrial apoptotic pathways and oxidative stress that holds great promise. |
| Databáze: | OpenAIRE |
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