ArticlePLoS biology2021
Extracellular DJ-1 induces sterile inflammation in the ischemic brain.
Article in PLoS biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Neurodegenerative diseases and immune system: From pathogenic mechanism to therapy.Neural regeneration research · 2026Article
- Neuroprotective Potential ofBiomolecules · 2026Article
- Blood-spinal cord barrier disruption after spinal cord injury: a time-dependent mechanistic review.Frontiers in cellular neuroscience · 2026Review
- Urea functions as a risk signal driving astrocyte-mediated neuroinflammation following stroke.Journal of neuroinflammation · 2025Article
- DJ-1 Promotes Diabetic Corneal Epithelial Wound Healing by Attenuating Hyperglycemia-Induced Oxidative Stress Through Inhibiting PTEN.Investigative ophthalmology & visual science · 2025Article
- Atorvastatin attenuates the expression of damage-associated molecular patterns and inflammatory cytokines in patients with psoriasis.Pharmacological reports : PR · 2025Article
- Betulin ameliorates neuronal apoptosis and oxidative injury via DJ-1/Akt/Nrf2 signaling pathway after subarachnoid hemorrhage.CNS neuroscience & therapeutics · 2024Article
- Differential Expression of Circulating Damage-Associated Molecular Patterns in Patients with Coronary Artery Ectasia.Biomolecules · 2023Article
- Identification of MYH9 as a key regulator for synoviocyte migration and invasion through secretome profiling.Annals of the rheumatic diseases · 2023Article
- Emergent Inflammatory Markers and Echocardiographic Indices in Patients with Bronchial Asthma.Biomolecules · 2023Article
- Role of alarmins in poststroke inflammation and neuronal repair.Seminars in immunopathology · 2023Review
- Neuroimmune mechanisms and therapies mediating post-ischaemic brain injury and repair.Nature reviews. Neuroscience · 2023Review
- DJ-1 Alleviates Neuroinflammation and the Related Blood-Spinal Cord Barrier Destruction by Suppressing NLRP3 Inflammasome Activation via SOCS1/Rac1/ROS Pathway in a Rat Model of Traumatic Spinal Cord Injury.Journal of clinical medicine · 2022Article
- Article
- Epithelial-Macrophage Crosstalk Initiates Sterile Inflammation in Embryonic Skin.Frontiers in immunology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is implicated in the onset and progression of various diseases, including cerebral pathologies. Here, we report that DJ-1, which plays a role within cells as an antioxidant protein, functions as a damage-associated molecular pattern (DAMP) and triggers inflammation if released from dead cells into the extracellular space. We first found that recombinant DJ-1 protein induces the production of various inflammatory cytokines in bone marrow-derived macrophages (BMMs) and dendritic cells (BMDCs). We further identified a unique peptide sequence in the αG and αH helices of DJ-1 that activates Toll-like receptor 2 (TLR2) and TLR4. In the ischemic brain, DJ-1 is released into the extracellular space from necrotic neurons within 24 h after stroke onset and makes direct contact with TLR2 and TLR4 in infiltrating myeloid cells. Although DJ-1 deficiency in a murine model of middle cerebral artery occlusion did not attenuate neuronal injury, the inflammatory cytokine expression in infiltrating immune cells was significantly decreased. Next, we found that the administration of an antibody to neutralize extracellular DJ-1 suppressed cerebral post-ischemic inflammation and attenuated ischemic neuronal damage. Our results demonstrate a previously unknown function of DJ-1 as a DAMP and suggest that extracellular DJ-1 could be a therapeutic target to prevent inflammation in tissue injuries and neurodegenerative diseases.
Indexed as
Identifiers
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.