Cited by 95Mitochondrial Function and PathologyAutophagy in Disease and TherapyCell death mechanisms and regulation

p53 and mitochondrial dysfunction: novel insight of neurodegenerative diseases

Open access
Dai, Chun-Qiu, Luo, Ting-Ting, Luo, Shi-Cheng, Wang, Jia-Qi, Wang, Sheng-Ming, Bai, Yun-Hu, Yang, Yan-Ling, Wang, Ya-Yun·2016·Journal of Bioenergetics and Biomembranes

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.

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Crossref · 10.1007/s10863-016-9669-5

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  • p53 can accumulate in the inner mitochondrial membrane and mediate the opening of MPTP in the inner mitochondrial membrane.

    “p53 can also accumulate in the inner mitochondrial membrane and mediate the opening of MPTP in the inner mitochondrial membrane [86].”

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Authors
Dai, C.-Q., Luo, T.-T., Luo, S.-C., Wang, J.-Q., Wang, S.-M., Bai, Y.-H., Yang, Y.-L., & Wang, Y.-Y.
Affiliations
  • Air Force Medical University (CN)
  • Xijing Hospital (CN)
Venue
Journal of Bioenergetics and Biomembranes
Published
2016-07-15
Volume
48
Issue
4
Pages
337-347
ISSN
  • 0145-479X (ISSN-L)
  • 1573-6881
OpenAlex
W2470044260
Cited by
93
References
48
Citations by year
2026: 3 · 2025: 9 · 2024: 14 · 2023: 9 · 2022: 12 · 2021: 10 · 2020: 13 · 2019: 8 · 2018: 7 · 2017: 8
FWCI
0.69
Type
journal article
Language
en
Open access
Locations
  • Journal of Bioenergetics and Biomembranes (publishedVersion, cc-by)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China (81272555, 81470843)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
p53, mitochondrial dysfunction, neurodegenerative diseases, SCO2, reactive oxygen species, mitochondrial degradation, apoptosis, necrosis, Parkinson's disease, Huntington's disease, Alzheimer's disease, targeted therapy
MeSH terms
Animals, Humans, Tumor Suppressor Protein p53, Neurodegenerative Diseases, Mitochondrial Diseases, Molecular Targeted Therapy

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