title: p53 and mitochondrial dysfunction: novel insight of neurodegenerative diseases.
abstract: Mitochondria are organelles responsible for vital cell functions. p53 is a transcription factor that regulates the DNA stability and cell growth normality. Recent studies revealed that p53 can influence mitochondrial function changing from normal condition to abnormal condition under different stress levels. In normal state, p53 can maintain mitochondrial respiration through transactivation of SCO2. When stress stimuli presents, SCO2 overexpresses and leads to ROS generation. ROS promotes p53 inducing MALM (Mieap-induced accumulation of lysosome-like organelles within mitochondria) to repair dysfunctional mitochondria and MIV (Mieap-induced vacuole) to accomplish damaged mitochondria degradation. If stress or damage is irreversible, p53 will translocate to mitochondria, leading into apoptosis or necrosis. Neurodegenerative diseases including Parkinson's disease, Huntington's disease and Alzheimer's disease are still lack of clear explanations of mechanisms, but more studies have revealed the functional relationship between mitochondria and p53 towards the pathological development of these diseases. In this review, we discuss that p53 plays the vital role in the function of mitochondria in the aspect of pathological change metabolism. We also analyze these diseases with novel targeted treating molecules which are related to p53 and mitochondria, hoping to present novel therapies in future clinic.
authors.affiliation: Department of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, The Fourth Military Medical University, Xi'an, 710032, China.
authors.forename: Chun-Qiu
authors.initials: CQ
authors.lastname: Dai
authors.affiliation: Department of Neurobiology and Collaborative Innovation Center for Brain Science, School of Basic Medicine, The Fourth Military Medical University, Xi'an, 710032, China.
authors.forename: Ting-Ting
authors.initials: TT
authors.lastname: Luo
authors.affiliation: Department of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, The Fourth Military Medical University, Xi'an, 710032, China.
authors.forename: Shi-Cheng
authors.initials: SC
authors.lastname: Luo
authors.affiliation: Department of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, The Fourth Military Medical University, Xi'an, 710032, China.
authors.forename: Jia-Qi
authors.initials: JQ
authors.lastname: Wang
authors.affiliation: Department of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, The Fourth Military Medical University, Xi'an, 710032, China.
authors.forename: Sheng-Ming
authors.initials: SM
authors.lastname: Wang
authors.affiliation: Department of Hepatobiliary Surgery, Xi-Jing Hospital, The Fourth Military Medical University, Xi'an, 710032, China.
authors.forename: Yun-Hu
authors.initials: YH
authors.lastname: Bai
authors.affiliation: Department of Hepatobiliary Surgery, Xi-Jing Hospital, The Fourth Military Medical University, Xi'an, 710032, China.
authors.forename: Yan-Ling
authors.initials: YL
authors.lastname: Yang
authors.affiliation: Department of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, The Fourth Military Medical University, Xi'an, 710032, China. Wang_YaYun_fmmu@163.com.
authors.forename: Ya-Yun
authors.initials: YY
authors.lastname: Wang
mesh_terms: D000818:Animals; D006801:Humans; D028361:Mitochondrial Diseases / Q000188:drug therapy / Q000378:metabolism*; D058990:Molecular Targeted Therapy / Q000379:methods; D019636:Neurodegenerative Diseases / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000502:physiology*
chemical_list: C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53
keywords: Apoptosis; Mitochondria; Mitochondrial dysfunction; Mitochondrial quality control; Molecular therapy; Neurodegenerative diseases; p53