ArticleCell death & disease2012
Impaired mitochondrial biogenesis contributes to depletion of functional mitochondria in chronic MPP+ toxicity: dual roles for ERK1/2.
Article in Cell death & disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.
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Who cites it
69 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
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- Superoxide signals for the mitophagy of dysfunctional mitochondria to maintain quality control.Redox biology · 2026Review
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- Exploring GPR120/FFAR4 pharmacology: Unveiling novel therapeutic avenues through molecular signaling pathways for Alzheimer's disease intervention.Brain, behavior, & immunity - health · 2025Review
- Sex-specific effects of chronic unpredictable stress on mitochondrial function in the HPA axis in mice.bioRxiv : the preprint server for biology · 2025Article
- Type 2 Diabetes Mellitus Exacerbates Pathological Processes of Parkinson's Disease: Insights from Signaling Pathways Mediated by Insulin Receptors.Neuroscience bulletin · 2025Review
- Association between mitochondrial DNA copy number and production traits in pigs.Journal of animal breeding and genetics = Zeitschrift fur Tierzuchtung und Zuchtungsbiologie · 2025Article
- The Role of Autophagy in Excitotoxicity, Synaptic Mitochondrial Stress and Neurodegeneration.Autophagy reports · 2025Article
- International consensus guidelines for the definition, detection, and interpretation of autophagy-dependent ferroptosis.Autophagy · 2024Review
- An AI-guided screen identifies probucol as an enhancer of mitophagy through modulation of lipid droplets.PLoS biology · 2023Article
- Pharmacological Progress of Mitophagy Regulation.Current neuropharmacology · 2023Article
- Evaluation of fisetin as a potential inducer of mitochondrial biogenesis in SH-SY5Y neuronal cells.Iranian journal of basic medical sciences · 2023Article
- Osthole attenuated cytotoxicity induced by 6-OHDA in SH-SY5Y cells through inhibition of JAK/STAT and MAPK pathways.Iranian journal of basic medical sciences · 2023Article
- Mitochondrial dysfunction-targeting therapeutics of natural products in Parkinson's disease.Frontiers in pharmacology · 2023Review
- Bacopa Protects against Neurotoxicity Induced by MPPMolecules (Basel, Switzerland) · 2022Article
- Vanillic acid induces mitochondrial biogenesis in SH-SY5Y cells.Molecular biology reports · 2022Article
- Mitochondria in neurodegeneration.Current opinion in physiology · 2022Article
9 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
6 authors at 4 institutions in 1 country.
Funding
Abstract
The regulation of mitochondrial quality has emerged as a central issue in neurodegeneration, diabetes, and cancer. We utilized repeated low-dose applications of the complex I inhibitor 1-methyl-4-phenylpyridinium (MPP(+)) over 2 weeks to study cellular responses to chronic mitochondrial stress. Chronic MPP(+) triggered depletion of functional mitochondria resulting in diminished capacities for aerobic respiration. Inhibiting autophagy/mitophagy only partially restored mitochondrial content. In contrast, inhibiting activation of extracellular signal-regulated protein kinases conferred complete cytoprotection with full restoration of mitochondrial functional and morphological parameters, enhancing spare respiratory capacity in MPP(+) co-treated cells above that of control cells. Reversal of mitochondrial injury occurred when U0126 was added 1 week after MPP(+), implicating enhanced repair mechanisms. Chronic MPP(+) caused a >90% decrease in complex I subunits, along with decreases in complex III and IV subunits. Decreases in respiratory complex subunits were reversed by co-treatment with U0126, ERK1/2 RNAi or transfection of dominant-negative MEK1, but only partially restored by degradation inhibitors. Chronic MPP(+) also suppressed the de novo synthesis of mitochondrial DNA-encoded proteins, accompanied by decreased expression of the mitochondrial transcription factor TFAM. U0126 completely reversed each of these deficits in mitochondrial translation and protein expression. These data indicate a key, limiting role for mitochondrial biogenesis in determining the outcome of injuries associated with elevated mitophagy.
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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.