Evidence map›Paper›PMID 27422544›Full record

ReviewJournal of bioenergetics and biomembranes2016

p53 and mitochondrial dysfunction: novel insight of neurodegenerative diseases.

Chun-Qiu Dai, Ting-Ting Luo, Shi-Cheng Luo, Jia-Qi Wang, Sheng-Ming Wang, Yun-Hu Bai, Yan-Ling Yang, Ya-Yun Wang

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of bioenergetics and biomembranes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.

  1. Pooled it
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  4. From environmental exposure to retinal pathology: epidemiological and mechanistic insights into multi-metal driven ocular diseases.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Chun-Qiu DaiDepartment of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, The Fourth Military Medical University, Xi'an, 710032, China.
Ting-Ting LuoDepartment of Neurobiology and Collaborative Innovation Center for Brain Science, School of Basic Medicine, The Fourth Military Medical University, Xi'an, 710032, China.
Shi-Cheng LuoDepartment of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, The Fourth Military Medical University, Xi'an, 710032, China.
Jia-Qi WangDepartment of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, The Fourth Military Medical University, Xi'an, 710032, China.
Sheng-Ming WangDepartment of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, The Fourth Military Medical University, Xi'an, 710032, China.
Yun-Hu BaiDepartment of Hepatobiliary Surgery, Xi-Jing Hospital, The Fourth Military Medical University, Xi'an, 710032, China.
Yan-Ling YangDepartment of Hepatobiliary Surgery, Xi-Jing Hospital, The Fourth Military Medical University, Xi'an, 710032, China.
Ya-Yun WangDepartment 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.
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AnimalsHumansMitochondrial DiseasesMolecular Targeted TherapyNeurodegenerative DiseasesTumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53ApoptosisMitochondriaMitochondrial dysfunctionMitochondrial quality controlMolecular therapyNeurodegenerative diseasesp53

Identifiers

PMID27422544
PMCPMC5026713
OpenAlexW2470044260

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.