ReviewFEBS letters2018
mPOS is a novel mitochondrial trigger of cell death - implications for neurodegeneration.
Review in FEBS letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
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Who cites it
29 citing papers in PubMed.
- A multilayered stress-response circuit: The mammalian mitochondrial UPR.The FEBS journal · 2026Review
- In and out of the mitochondrial intermembrane space.Protein science : a publication of the Protein Society · 2026Review
- Interaction of lncRNA LENT with DHX36 regulates translation and suppresses autophagy in melanoma.Cell death & disease · 2025Article
- Improved AAV9-based gene therapy design forMolecular therapy. Methods & clinical development · 2025Article
- Mitochondrial protein import stress augments α-synuclein aggregation and neural damage independent of bioenergetics.Research square · 2025Article
- Single-cell proteomics reveals decreased abundance of proteostasis and meiosis proteins in advanced maternal age oocytes.Molecular human reproduction · 2024Article
- Mitochondrial stress: a key role of neuroinflammation in stroke.Journal of neuroinflammation · 2024Review
- Article
- Adenine nucleotide carrier protein dysfunction in human disease.IUBMB life · 2023Review
- Mitochondrial dysfunction rapidly modulates the abundance and thermal stability of cellular proteins.Life science alliance · 2023Article
- Article
- Defective import of mitochondrial metabolic enzyme elicits ectopic metabolic stress.Science advances · 2023Article
- The Journey of Mitochondrial Protein Import and the Roadmap to Follow.International journal of molecular sciences · 2023Review
- Early growth response-1: Key mediators of cell death and novel targets for cardiovascular disease therapy.Frontiers in cardiovascular medicine · 2023Review
- The emergent role of mitochondrial surveillance in cellular health.Aging cell · 2022Review
- Cytosolic adaptation to mitochondria-induced proteostatic stress causes progressive muscle wasting.iScience · 2022Article
- Altered Mitochondrial Protein Homeostasis and Proteinopathies.Frontiers in molecular neuroscience · 2022Review
- Article
- Cytosolic Quality Control of Mitochondrial Protein Precursors-The Early Stages of the Organelle Biogenesis.International journal of molecular sciences · 2021Review
- Mitochondrial stress response in drug-induced liver injury.Molecular biology reports · 2021Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
In addition to its central role in energy metabolism, the mitochondrion has many other functions essential for cell survival. When stressed, the multifunctional mitochondria are expected to engender multifaceted cell stress with complex physiological consequences. Potential extra-mitochondrial proteostatic burdens imposed by inefficient protein import have been largely overlooked. Accumulating evidence suggests that a diverse range of pathogenic mitochondrial stressors, which do not directly target the core protein import machinery, can reduce cell fitness by disrupting the proteostatic network in the cytosol. The resulting stress, named mitochondrial precursor overaccumulation stress (mPOS), is characterized by the toxic accumulation of unimported mitochondrial proteins in the cytosol. Here, we review our current understanding of how mitochondrial dysfunction can impact the cytosolic proteome and proteostatic signaling. We also discuss the intriguing possibility that the mPOS model may help untangle the cause-effect relationship between mitochondrial dysfunction and cytosolic protein aggregation, which are probably the two most prominent molecular hallmarks of neurodegenerative disease.
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What OpenQuestion holds
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.