ReviewFrontiers in medicine2022
Immune dysfunction following severe trauma: A systems failure from the central nervous system to mitochondria.
Review in Frontiers in medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
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Who cites it
29 citing papers in PubMed, 39 citations in OpenAlex.
- Pathophysiology-guided biomarkers and therapeutics for precision trauma medicine in polytrauma with musculoskeletal injuries.Military Medical Research · 2026Review
- Inflammation-linked adipokine profiles associate with acute organ dysfunction after severe trauma.Journal of translational medicine · 2026Article
- Endocrine disruptions in thermal injuries: exploring immune system interactions.Physiological reviews · 2026Review
- Regulatory T cell attracting therapy accelerates skeletal muscle functional recovery following injury.Scientific reports · 2026Article
- Epigenome-wide analysis of DNA-methylation signatures following climate-related disasters.BMC medicine · 2026Article
- Article
- ALM Resuscitation Without Transfusion Improves Platelet Function and Survival After Liver Injury and Uncontrolled Hemorrhage.Medicina (Kaunas, Lithuania) · 2026Article
- Article
- Beyond wound closure: translational opportunities and barriers of mesenchymal stem cells and their extracellular vesicles in burn management.Frontiers in cell and developmental biology · 2026Review
- Risk factors for postoperative cognitive dysfunction in geriatric trauma: a dual-pathway perspective.Frontiers in aging neuroscience · 2026Article
- Limited Utility of the CALLY Index in Enhancing Mortality Prediction for Trauma Patients in Intensive Care Units: A Retrospective Analysis.Risk management and healthcare policy · 2026Article
- Mitochondrial dysfunction in immune cells during the perioperative period: mechanisms, emerging therapeutic strategies, and implications for multi-organ protection.Frontiers in immunology · 2026Review
- Molecular Mechanisms of Transfusion-Associated Immunomodulation and Its Impact in the Critically Ill.International journal of molecular sciences · 2025Review
- Wound-Healing Potential of Engineered Lysin GRC-ML07 inAntibiotics (Basel, Switzerland) · 2025Article
- Early prediction and warning of MODS following major trauma via identification of cytokine storm: A prospective cohort study.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2025Article
- Kidneys on the Frontline: Nephrologists Tackling the Wilds of Acute Kidney Injury in Trauma Patients-From Pathophysiology to Early Biomarkers.Diagnostics (Basel, Switzerland) · 2025Review
- Fibrinogen based resuscitation mitigates lung injury in mice with bacterial pneumonia after hemorrhagic shock.Biochemistry and biophysics reports · 2025Article
- Identifying early predictive and diagnostic biomarkers and exploring metabolic pathways for sepsis after trauma based on an untargeted metabolomics approach.Scientific reports · 2025Article
- The Intersection of Trauma and Immunity: Immune Dysfunction Following Hemorrhage.Biomedicines · 2024Review
- Monitoring Immune Dysfunction in Critically Ill Patients with Carbapenem-ResistantAntibiotics (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When a traumatic injury exceeds the body's internal tolerances, the innate immune and inflammatory systems are rapidly activated, and if not contained early, increase morbidity and mortality. Early deaths after hospital admission are mostly from central nervous system (CNS) trauma, hemorrhage and circulatory collapse (30%), and later deaths from hyperinflammation, immunosuppression, infection, sepsis, acute respiratory distress, and multiple organ failure (20%). The molecular drivers of secondary injury include damage associated molecular patterns (DAMPs), pathogen associated molecular patterns (PAMPs) and other immune-modifying agents that activate the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic stress response. Despite a number of drugs targeting specific anti-inflammatory and immune pathways showing promise in animal models, the majority have failed to translate. Reasons for failure include difficulty to replicate the heterogeneity of humans, poorly designed trials, inappropriate use of specific pathogen-free (SPF) animals, ignoring sex-specific differences, and the flawed practice of single-nodal targeting. Systems interconnectedness is a major overlooked factor. We argue that if the CNS is protected early after major trauma and control of cardiovascular function is maintained, the endothelial-glycocalyx will be protected, sufficient oxygen will be delivered, mitochondrial energetics will be maintained, inflammation will be resolved and immune dysfunction will be minimized. The current challenge is to develop new systems-based drugs that target the CNS coupling of whole-body function.
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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.