ArticleBehavioural brain research2013
Behavioral effects of SQSTM1/p62 overexpression in mice: support for a mitochondrial role in depression and anxiety.
Article in Behavioural brain research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- Review
- Mitochondrial dysfunction in psychiatric disorders.Schizophrenia research · 2024Review
- Article
- Article
- Review
- The role of SQSTM1 (p62) in mitochondrial function and clearance in human cortical neurons.Stem cell reports · 2021Article
- Mitophagy in Human Diseases.International journal of molecular sciences · 2021Review
- Molecular markers of neuroendocrine function and mitochondrial biogenesis associated with early life stress.Psychoneuroendocrinology · 2020Article
- KEAP1-NRF2 signalling and autophagy in protection against oxidative and reductive proteotoxicity.The Biochemical journal · 2015Review
- Emerging functional cross-talk between the Keap1-Nrf2 system and mitochondria.Journal of clinical biochemistry and nutrition · 2015Review
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Affective spectrum and anxiety disorders have come to be recognized as the most prevalently diagnosed psychiatric disorders. Among a suite of potential causes, changes in mitochondrial energy metabolism and function have been associated with such disorders. Thus, proteins that specifically change mitochondrial functionality could be identified as molecular targets for drugs related to treatment for affective spectrum disorders. Here, we report generation of transgenic mice overexpressing the scaffolding and mitophagy related protein Sequestosome1 (SQSTM1/p62) or a single point mutant (P392L) in the UBA domain of SQSTM1/p62. We show that overexpression of SQSTM1/p62 increases mitochondrial energy output and improves transcription factor import into the mitochondrial matrix. These elevated levels of mitochondrial functionality correlate directly with discernible improvements in mouse behaviors related to affective spectrum and anxiety disorders. We also describe how overexpression of SQSTM1/p62 improves spatial learning and long term memory formation in these transgenic mice. These results suggest that SQSTM1/p62 provides an attractive target for therapeutic agents potentially suitable for the treatment of anxiety and affective spectrum disorders.
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Registered trials
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.