RETRACTED ARTICLE: Parkin and PINK1 mitigate STING-induced inflammation
Open accessAbstract
Although serum from patients with Parkinson's disease contains elevated levels of numerous pro-inflammatory cytokines including IL-6, TNF, IL-1β, and IFNγ, whether inflammation contributes to or is a consequence of neuronal loss remains unknown 1. Mutations in parkin, an E3 ubiquitin ligase, and PINK1, a ubiquitin kinase, cause early onset Parkinson's disease 2,3. Both PINK1 and parkin function within the same biochemical pathway and remove damaged mitochondria from cells in culture and in animal models via mitophagy, a selective form of autophagy 4. The in vivo role of mitophagy, however, is unclear, partly because mice that lack either PINK1 or parkin have no substantial Parkinson's-disease-relevant phenotypes 5-7. Mitochondrial stress can lead to the release of damage-associated molecular patterns (DAMPs) that can activate innate immunity 8-12, suggesting that mitophagy may mitigate inflammation. Here we report a strong inflammatory phenotype in both Prkn-/- and Pink1-/- mice following exhaustive exercise and in Prkn-/-;mutator mice, which accumulate mutations in mitochondrial DNA (mtDNA)13,14. Inflammation resulting from either exhaustive exercise or mtDNA mutation is completely rescued by concurrent loss of STING, a central regulator of the type I interferon response to cytosolic DNA 15,16. The loss of dopaminergic neurons from the substantia nigra pars compacta and the motor defect observed in aged Prkn-/-;mutator mice are also rescued by loss of STING, suggesting that inflammation facilitates this phenotype. Humans with mono- and biallelic PRKN mutations also display elevated cytokines. These results support a role for PINK1- and parkin-mediated mitophagy in restraining innate immunity.
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Loss of PRKN and PINK1 dysregulates mitophagy and increases mitochondria stress, leading to mito-inflammation, which is involved in PD pathology in PINK1 and PRKN deficient mice.
“Multiple studies have revealed that loss of PRKN and PINK1 dysregulated mitophagy and increased mitochondria stress, leading to mito-inflammation,267 which was recently suggested to be involved in PD pathology in PINK1 and PRKN deficient mice.268”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [268]
The paper’s Abstract reports inflammation after mitochondrial stress in both PINK1- and Parkin-deficient mice and proposes that this pathway may contribute to Parkinson’s disease. But it reports dopaminergic neuron loss and a motor defect only in aged Parkin-deficient Mutator mice; it also says mice lacking PINK1 or Parkin alone have no substantial PD-relevant phenotypes. The claim therefore extends the reported PD-like pathology to PINK1-deficient mice. (LLM, conf=0.87)
Experimental — accuracy not yet measuredKnockout of STING reverses motor deficit and neuron loss in aged PRKN knockout PD mouse model.
“Knockout of STING reverses motor deficit and neuron loss in aged PRKN knockout PD mouse model.268”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [268]
The paper reports that loss of STING rescued the motor defect and dopaminergic neuron loss in aged Parkin−/−;Mutator mice (passage 1). The claim omits the Mutator background, which matters: the paper says mice lacking Parkin alone have no substantial PD-relevant phenotype (passage 3). (LLM, conf=0.86)
Experimental — accuracy not yet measuredPeripheral dysregulation of IFN production is linked with the pathogenesis of CNS neurodegenerative conditions.
“peripheral dysregulation of IFN production is linked with the pathogenesis of CNS neurodegenerative conditions.”
From Interferon signaling modulates Down syndrome-associated Alzheimer’s disease pathology in a mouse model (2025) · cites this paper as [84]
The Abstract reports elevated serum IFNβ1 in a Parkinson’s-disease mouse model and says that loss of STING rescued both the inflammatory response and dopaminergic-neuron loss, suggesting a link. It does not establish this link across CNS neurodegenerative conditions generally, and it says whether inflammation contributes to neuronal loss in human Parkinson’s disease remains unknown. No page number is provided in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThere is notable convergence on cGAS-STING signalling in chronic neurodegenerative conditions across our study and previous studies in models of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and frontotemporal dementia, and Nieman-Pick's disease.
“Together with previous studies in models of Alzheimer’s disease53, Parkinson’s disease54,55, amyotrophic lateral sclerosis and frontotemporal dementia56, and Nieman–Pick’s disease57, our study reveals notable convergence on cGAS–STING signalling in chronic neurodegenerative conditions.”
From cGAS–STING drives ageing-related inflammation and neurodegeneration (2023) · cites this paper as [54]
Genetic and pharmacological restoration of autophagic/mitophagic clearance in animal models of neurodegenerative diseases ameliorates disease-defining pathologies and behavioral deficits.
“Genetic and pharmacological restorations of autophagic/mitophagic clearance in animal models of these diseases ameliorate disease-defining pathologies and behavioral deficits (Fang et al., 2019; Ravikumar et al., 2004; Sliter et al., 2018).”
From NAD+ in Brain Aging and Neurodegenerative Disorders (2019) · cites this paper as Sliter et al., 2018
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“Multiple studies have revealed that loss of PRKN and PINK1 dysregulated mitophagy and increased mitochondria stress, leading to mito-inflammation,(267) which was recently suggested to be involved in PD pathology in PINK1 and PRKN deficient mice.(268) In addition to mito-inflammation, both PRKN and PINK1 have been impl…”
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Self-citation
- Authors
- Sliter, D. A., Martinez, J., Hao, L., Chen, X., Sun, N., Fischer, T. D., Burman, J. L., Li, Y., Zhang, Z., Narendra, D. P., Cai, H., Borsche, M., Klein, C., & Youle, R. J.
- Affiliations
- National Institutes of Health (US)
- University of Lübeck (DE)
- Corresponding author
- Youle, Richard J.
- ORCID
- Venue
- Nature
- Published
- 2018-08-22
- Volume
- 561
- Issue
- 7722
- Pages
- 258-262
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC7362342
- OpenAlex
- W2887997888
- Cited by
- 1,287
- References
- 39
- Citations by year
- 2026: 68 · 2025: 177 · 2024: 190 · 2023: 185 · 2022: 180 · 2021: 197 · 2020: 157 · 2019: 115 · 2018: 16
- FWCI
- 82.18
- Type
- journal article
- Language
- en
- Status
- Retracted
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (DFG FOR2488)
- National Institute of Neurological Disorders and Stroke (Z01NS002859, ZIANS002859)
- National Institute of Environmental Health Sciences (1ZIAES10328601, ZIAES103286)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Keywords
- Parkin, PINK1, STING, mitophagy, Parkinson's disease, neuroinflammation, mitochondrial DNA mutations, exhaustive exercise, innate immunity, dopaminergic neurons, substantia nigra pars compacta, motor impairment, type I interferon response, cytosolic DNA, E3 ubiquitin ligase
- MeSH terms
- Alarmins, STING Protein, PTEN-Induced Putative Kinase, Animals, DNA, Mitochondrial, Humans, Immunity, Innate, Inflammation, Membrane Proteins, Mice, Inbred C57BL, Parkinson Disease, Physical Conditioning, Animal, Protein Kinases, Stress, Physiological, Ubiquitin-Protein Ligases, Mice, Receptor, Interferon alpha-beta, Mitophagy
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