ReviewNeurotoxicity research2021
Sepsis and Cerebral Dysfunction: BBB Damage, Neuroinflammation, Oxidative Stress, Apoptosis and Autophagy as Key Mediators and the Potential Therapeutic Approaches.
Review in Neurotoxicity research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 2 of them syntheses that pooled it.
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
119 citing papers in PubMed, 2 syntheses or guidelines pooled it, 198 citations in OpenAlex.
- Environmental epigenetic modifiers in neurodegenerative diseases: a systematic review of epigenomic mechanisms and therapeutic targets.Frontiers in epigenetics and epigenomics · 2026Pooled it
- Zingerone as a Neuroprotective Agent Against Cognitive Disorders: A Systematic Review of Preclinical Studies.International journal of molecular sciences · 2025Pooled it
- DietaryJournal of microbiology and biotechnology · 2026Article
- Barbaloin Attenuates Cisplatin-Induced Hippocampal Neurotoxicity by Suppressing Oxidative Stress, Neuroinflammation, and Apoptosis: In Vivo and In Silico Evidence.Journal of biochemical and molecular toxicology · 2026Article
- Gut‑brain axis in anesthesia and critical illness: Molecular crosstalk and its impact on delirium and outcome (Review).International journal of molecular medicine · 2026Review
- ARISE framework: a temporal, multi-organ view of perfusion in sepsis.Internal and emergency medicine · 2026Review
- Hippocampal cytopathology orchestrates post-septic cognitive dysfunction.Metabolic brain disease · 2026Review
- Cel-LDH dual-functional nanotherapy simultaneously promotes microglial efferocytosis and alleviates neuronal apoptosis for spinal cord injury recovery.Journal of nanobiotechnology · 2026Article
- Impact of prenatal LPS on sepsis-related neurobiological outcomes.Metabolic brain disease · 2026Article
- Roles of gut and oral microbiota in methamphetamine-induced multi-organ toxicity.Cell biology and toxicology · 2026Review
- Effects of Lactate on Improving Cognitive Function and Survival Rate in a Mouse Model of Post-Sepsis Cognitive Impairment.Actas espanolas de psiquiatria · 2026Article
- Detection of inflammation-related blood-brain barrier dysfunction using PET and MR imaging: a pilot study.Scientific reports · 2026Article
- Endothelial-specific Ezh2 deficiency exacerbates blood-brain barrier dysfunction and neuroinflammation in sepsis-associated encephalopathy.Journal of neuroinflammation · 2026Article
- Angiotensin-(1-7) suppresses pyroptosis in cerebral endothelium to decrease blood-brain barrier permeability and cognitive impairments in sepsis.The Journal of international medical research · 2026Article
- Maresin-1 Alleviates Sepsis-Induced Liver Injury by Regulating Apoptosis and Autophagy via Activation of the PI3K/Akt Signaling Pathway in Mice.Current issues in molecular biology · 2026Article
- Neuropathologic Autopsy Findings in Pediatric Sepsis: A Two-Center, Retrospective Study.Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies · 2026Article
- Article
- Liraglutide alleviates sepsis-associated encephalopathy via attenuating neuronal damage, glial cell activation and mitochondrial dysfunction in a mouse model of sepsis.European journal of medical research · 2026Article
- α7nAChR alleviates cognitive impairment by promoting autophagy in astrocytes via CaMKK2/AMPK/mTOR pathway in sepsis-associated encephalopathy.Frontiers in immunology · 2026Article
- Unveiling the neuroprotective effects of pomegranate extract and/or physical activity against aluminum chloride-induced Alzheimer's disease in rats: modulation of multitude pathways.Frontiers in pharmacology · 2026Article
59 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
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-associated cerebral dysfunction is complex pathophysiology, generated from primary infections that are developed elsewhere in the body. The neonates, elderly population and chronically ill and long-term hospitalized patients are predominantly vulnerable to sepsis and related cerebral damage. Generally, electrophysiological recordings, severity and sedation scales, computerized imaging and spectroscopy techniques are used for its detection and diagnosis. About the underlying mechanisms, enhanced blood-brain barrier permeability and metalloprotease activity, tight junction protein loss and endothelial cell degeneration promote the influx of inflammatory and toxic mediators into the brain, triggering cerebrovascular damage. An altered neutrophil count and phenotype further dysregulate the normal neuroimmune responses and neuroendocrine stability via modulated activation of protein kinase C-delta, nuclear factor kappa-B and sphingolipid signaling. Glial activation, together with pro-inflammatory cytokines and chemokines and the Toll-like receptor, destabilize the immune system. Moreover, superoxides and hydroperoxides generate oxidative stress and perturb mitochondrial dynamics and ATP synthesis, propagating neuronal injury cycle. Activated mitochondrial apoptotic pathway, characterized by increased caspase-3 and caspase-9 cleavage and Bax/Bcl2 ratio in the hippocampal and cortical neurons, stimulate neurocognitive impairments. Additionally, altered LC3-II/I and P62/SQSTM1, p-mTOR, p-AMPK1 and p-ULK1 levels and dysregulated autophagosome-lysosome fusion decrease neuronal and glial energy homeostasis. The therapies and procedures for attenuating sepsis-induced brain damage include early resuscitation, cerebral blood flow autoregulation, implantable electric vagus nerve stimulation, antioxidants, statins, glucocorticoids, neuroimmune axis modulators and PKCδ inhibitors. The current review enumerates the pathophysiology of sepsis-induced brain damage, its diagnosis, the role of critical inducers and mediators and, ultimately, therapeutic measures attenuating cerebrovascular degeneration.
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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 Socratic graph.