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Mitochondrial dysfunction in neurodegenerative diseases and drug targets via apoptotic signaling.
Mitochondrion. 2019 11; 49:35-45.M

Abstract

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.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Wu Y
Department of Neurology, Anhui Provincial Hospital, Anhui Medical University, Hefei, Anhui Province 230001, PR China; Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, PR China.
Chen M
Department of Neurology, Anhui Provincial Hospital, Anhui Medical University, Hefei, Anhui Province 230001, PR China.
Jiang J
Department of Nephrology, Anhui Provincial Hospital, Anhui Medical University, Hefei, Anhui Province 230001, PR China; Department of Nephrology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, PR China. Electronic address: jiangjielong01@163.com.

MeSH

AnimalsApoptosisHumansMitochondriaNeurodegenerative DiseasesOxidative StressSignal Transduction

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

31288090

Citation

Wu, Yuanbo, et al. "Mitochondrial Dysfunction in Neurodegenerative Diseases and Drug Targets Via Apoptotic Signaling." Mitochondrion, vol. 49, 2019, pp. 35-45.
Wu Y, Chen M, Jiang J. Mitochondrial dysfunction in neurodegenerative diseases and drug targets via apoptotic signaling. Mitochondrion. 2019;49:35-45.
Wu, Y., Chen, M., & Jiang, J. (2019). Mitochondrial dysfunction in neurodegenerative diseases and drug targets via apoptotic signaling. Mitochondrion, 49, 35-45. https://doi.org/10.1016/j.mito.2019.07.003
Wu Y, Chen M, Jiang J. Mitochondrial Dysfunction in Neurodegenerative Diseases and Drug Targets Via Apoptotic Signaling. Mitochondrion. 2019;49:35-45. PubMed PMID: 31288090.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondrial dysfunction in neurodegenerative diseases and drug targets via apoptotic signaling. AU - Wu,Yuanbo, AU - Chen,Meiqiao, AU - Jiang,Jielong, Y1 - 2019/07/06/ PY - 2019/01/21/received PY - 2019/05/24/revised PY - 2019/07/05/accepted PY - 2019/7/10/pubmed PY - 2020/5/7/medline PY - 2019/7/10/entrez KW - Mitochondrial apoptotic pathway KW - Mitochondrial dysfunction KW - Neurodegenerative disorder KW - Oxidative stress and neuroprotection SP - 35 EP - 45 JF - Mitochondrion JO - Mitochondrion VL - 49 N2 - 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. SN - 1872-8278 UR - https://www.unboundmedicine.com/medline/citation/31288090/Mitochondrial_dysfunction_in_neurodegenerative_diseases_and_drug_targets_via_apoptotic_signaling_ DB - PRIME DP - Unbound Medicine ER -