ArticleAutophagy2020
Extracellular SQSTM1 as an inflammatory mediator.
Article in Autophagy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
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.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Glycosylation modulation as a therapeutic strategy for neuroinflammatory disorders: The potential of Tanshinone IIA.iScience · 2026Article
- ChIP-seq and RNA-seq Reveal the Involvement of Histone Lactylation Modification in Early Pregnancy with Subclinical Hypothyroidism.Biochemical genetics · 2026Article
- Gasdermin D-driven pyroptosis in sepsis: mechanisms, therapeutic strategies, and clinical translation.Frontiers in immunology · 2026Review
- EGb761 suppressed vascular dementia via modulating Wnt/β-catenin signaling pathway-induced apoptosis and autophagy in hippocampal neuronal cells.European journal of medical research · 2025Article
- Insights on the crosstalk among different cell death mechanisms.Cell death discovery · 2025Review
- NFκB1: a common biomarker linking Alzheimer's and Parkinson's disease pathology.Frontiers in neuroscience · 2025Article
- In pre-clinical study fetal hypoxia caused autophagy and mitochondrial impairment in ovary granulosa cells mitigated by melatonin supplement.Journal of advanced research · 2024Article
- The lipid basis of cell death and autophagy.Autophagy · 2024Review
- Article
- Review
- Repurposing Simvastatin in Parkinson's Disease Model: Protection Is throughout Modulation of the Neuro-Inflammatory Response in theInternational journal of molecular sciences · 2023Article
- Review
- Extracellular SQSTM1 exacerbates acute pancreatitis by activating autophagy-dependent ferroptosis.Autophagy · 2023Article
- Autophagy modulators influence the content of important signalling molecules in PS-positive extracellular vesicles.Cell communication and signaling : CCS · 2023Article
- Pyroptosis, ferroptosis, and autophagy cross-talk in glioblastoma opens up new avenues for glioblastoma treatment.Cell communication and signaling : CCS · 2023Review
- TREM2 inhibition triggers antitumor cell activity of myeloid cells in glioblastoma.Science advances · 2023Article
- scDual-Seq ofFrontiers in immunology · 2023Article
- Frameshift mutation in SQSTM1 causes proximal myopathy with rimmed vacuoles: A case report.Frontiers in neurology · 2023Article
- NLRP3 inflammasome activation in cigarette smoke priming for Pseudomonas aeruginosa-induced acute lung injury.Redox biology · 2022Article
- The STING1-MYD88 complex drives ACOD1/IRG1 expression and function in lethal innate immunity.iScience · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Excessive inflammation may lead to irreparable injury and even death, but the key mediators and underlying mechanisms remain unclear. Our recent findings indicate that SQSTM1/p62 (sequestosome 1), a well-known macroautophagy/autophagy receptor, is a lethal inflammatory mediator of sepsis and septic shock. The release of SQSTM1 occurs during tissue damage or microbial invasion through two main ways: one is passive and the other is active. Passive release occurs in the context of GSDMD-mediated pyroptosis. Active SQSTM1 secretion requires two basic steps: the first step is the expression and phosphorylation of SQSTM1 mediated by STING1/STING/TMEM173, and then the unconventional secretion of SQSTM1 by secretory lysosomes. After release, the extracellular SQSTM1 binds to membrane receptor INSR to activate glycolysis, leading to subsequent production of pro-inflammatory cytokines in a transcription factor NFKB-dependent manner. Functionally, genetic deletion or pharmacological inhibition of the SQSTM1-INSR pathway limits tissue damage, systemic inflammation, organ failure, and death in experimental sepsis models in mice. Moreover, the activation of the SQSTM1-INSR pathway is related to the severity of sepsis in patients. These findings highlight a pathological role of extracellular SQSTM1 in infection, inflammation, and immunity.
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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.