ArticleAutophagy2013
The accumulation of misfolded proteins in the mitochondrial matrix is sensed by PINK1 to induce PARK2/Parkin-mediated mitophagy of polarized mitochondria.
Article in Autophagy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 231 papers, 2 of them syntheses that pooled it.
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
231 citing papers in PubMed, 2 syntheses or guidelines pooled it, 408 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- CLPX acquires an iron-sulfur cluster to sustain mitochondrial proteostasis in cancer cells.Nature communications · 2026Article
- Quality control of protein import into mammalian mitochondria.Protein science : a publication of the Protein Society · 2026Review
- Targeting of kinases to treat neurodegenerative diseases.Pharmacological reviews · 2026Review
- Two Routes for Removing Unhealthy Mitochondria: Degradation and Secretion.Circulation research · 2026Review
- The integrated stress response suppresses PINK1-dependent mitophagy by preserving mitochondrial import efficiency.Nature communications · 2026Article
- Mitochondrial ROS in Retinal Neurodegeneration: Thresholds, Quality Control Failure, and Precision Therapeutic Windows.Biomolecules · 2026Review
- Structural remodeling of the mitochondrial protein biogenesis machinery under proteostatic stress.Science advances · 2026Article
- Bnip3lb-driven mitophagy maintains fate of the embryonic hematopoietic stem cell pool.Nature communications · 2026Article
- Reversing Mitochondrial Dysfunction in Optineurin E50K Glaucoma: A Metabolic Approach to Neuroprotection.Research square · 2026Article
- Mitophagy in pancreatic cancer: mechanistic insights and implications for novel therapeutic strategies.Cell death discovery · 2026Review
- Cis or trans: a puzzle of Parkin activation mechanism.Essays in biochemistry · 2026Review
- Targeting VCP with V8 suppresses glioblastoma development via formation of aggregates and disruption of mitophagy flux.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Novel insight into PINK1/parkin-associated autophagy implicated in Parkinson disease.Translational neuroscience · 2026Review
- When mitochondria lose their fold: matrix proteostasis and stress signaling.Frontiers in physiology · 2026Review
- Comprehensive analysis of mitochondrial unfolded protein response related genes for prognosis and therapeutic response in pancreatic cancer.Frontiers in immunology · 2026Article
- A unified mechanism for mitochondrial damage sensing in PINK1-Parkin-mediated mitophagy.The EMBO journal · 2026Article
- Mitochondrial protein import stress in Parkinson's disease: the TOM/TIM-PINK1/Parkin-DELE1/HRI axis linking mitochondrial proteostasis to neuronal death.Frontiers in cell and developmental biology · 2026Review
- Geniposide Attenuates Post-Myocardial Infarction Cardiac RemodelingCurrent medicinal chemistry · 2026Article
171 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Defective mitochondria exert deleterious effects on host cells. To manage this risk, mitochondria display several lines of quality control mechanisms: mitochondria-specific chaperones and proteases protect against misfolded proteins at the molecular level, and fission/fusion and mitophagy segregate and eliminate damage at the organelle level. An increase in unfolded proteins in mitochondria activates a mitochondrial unfolded protein response (UPR(mt)) to increase chaperone production, while the mitochondrial kinase PINK1 and the E3 ubiquitin ligase PARK2/Parkin, whose mutations cause familial Parkinson disease, remove depolarized mitochondria through mitophagy. It is unclear, however, if there is a connection between those different levels of quality control (QC). Here, we show that the expression of unfolded proteins in the matrix causes the accumulation of PINK1 on energetically healthy mitochondria, resulting in mitochondrial translocation of PARK2, mitophagy and subsequent reduction of unfolded protein load. Also, PINK1 accumulation is greatly enhanced by the knockdown of the LONP1 protease. We suggest that the accumulation of unfolded proteins in mitochondria is a physiological trigger of mitophagy.
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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.