ArticleNeurotoxicity research2021
Stanniocalcin 1 Inhibits the Inflammatory Response in Microglia and Protects Against Sepsis-Associated Encephalopathy.
Article in Neurotoxicity research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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
16 citing papers in PubMed, 48 citations in OpenAlex.
- Mitochondrial dysfunction, neuroinflammation, and associated mechanisms in sepsis-associated encephalopathy: from pathogenesis to emerging therapeutics.Frontiers in neuroscience · 2026Review
- AAV-mediated STC-1 expression mitigates neuroinflammation and preserves visual function in degenerative retinopathy.Journal of translational medicine · 2025Article
- Review on the Role of Mitochondrial Dysfunction in Septic Encephalopathy.Cell biochemistry and biophysics · 2025Review
- miR-208a-3p discriminates osteoporosis, predicts fracture, and regulates osteoclast activation through targeting STC1.Journal of orthopaedic surgery and research · 2025Article
- Ubiquitin-Specific Protease 8 Regulates Cognitive Dysfunction of Mice with Sepsis-Associated Encephalopathy Through SIRT1 Deubiquitination.Current neurovascular research · 2025Article
- MSCs promote the efferocytosis of large peritoneal macrophages to eliminate ferroptotic monocytes/macrophages in the injured endometria.Stem cell research & therapy · 2024Article
- A Prospective Longitudinal Cohort Study of Serum Stanniocalcin-1 as a Potential Prognostic Biomarker of Severe Traumatic Brain Injury.Therapeutics and clinical risk management · 2024Article
- Microglial Activation: Key Players in Sepsis-Associated Encephalopathy.Brain sciences · 2023Review
- Exploring Neuroprotective Agents for Sepsis-Associated Encephalopathy: A Comprehensive Review.International journal of molecular sciences · 2023Review
- Usability of Serum Stanniocalcin-1 as a Prognostic Biochemical Marker of Acute Supratentorial Intracerebral Hemorrhage: A Prospective Cohort Study.International journal of general medicine · 2023Article
- Selenoproteins and the senescence-associated epitranscriptome.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Exosomes from Adipose Mesenchymal Stem Cells Overexpressing Stanniocalcin-1 Promote Reendothelialization After Carotid Endarterium Mechanical Injury.Stem cell reviews and reports · 2022Article
- Insight Into Regulatory T Cells in Sepsis-Associated Encephalopathy.Frontiers in neurology · 2022Review
- Central role of microglia in sepsis-associated encephalopathy: From mechanism to therapy.Frontiers in immunology · 2022Review
- (-)-Epicatechin Reduces Neuroinflammation, Protects Mitochondria Function, and Prevents Cognitive Impairment in Sepsis-Associated Encephalopathy.Oxidative medicine and cellular longevity · 2022Article
- Stanniocalcin-1 Protected Astrocytes from Hypoxic Damage Through the AMPK Pathway.Neurochemical research · 2021Article
Corrections and comments
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Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-associated encephalopathy is a serious consequence of sepsis, triggered by the host response against an infectious agent, that can lead to brain damage and cognitive impairment. Several mechanisms have been proposed in this bidirectional communication between the immune system and the brain after sepsis as neuroinflammation, oxidative stress, and mitochondrial dysfunction. Stanniocalcin-1 (STC-1), an endogen neuroprotective protein, acts as an anti-inflammatory and suppresses superoxide generation through induction of uncoupling proteins (UCPs) in the mitochondria. Here, we demonstrated a protective role of STC-1 on inflammatory responses in vitro, in activated microglia stimulated with LPS, and on neuroinflammation, oxidative stress, and mitochondrial function in the hippocampus of rats subjected to an animal model of sepsis by cecal ligation and puncture (CLP), as well the consequences on long-term memory. Recombinant human STC-1 (rhSTC1) suppressed the pro-inflammatory cytokine production in LPS-stimulated microglia without changing the UCP-2 expression. Besides, rhSTC1 injected into the cisterna magna decreased acute hippocampal inflammation and oxidative stress and increased the activity of complex I and II activity of mitochondrial respiratory chain and creatine kinase at 24 h after sepsis. rhSTC1 was effective in preventing long-term cognitive impairment after CLP. In conclusion, rhSTC1 confers significant neuroprotection by inhibiting the inflammatory response in microglia and protecting against sepsis-associated encephalopathy in rats.
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