ReviewAging and disease2025
Immunosenescence in Sepsis: Molecular Mechanisms and Potential Therapeutic Targets.
Review in Aging and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis 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
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Assessing Monoclonal and Polyclonal Antibodies in Sepsis and Septic Shock: A Systematic Review of Efficacy and Safety.International journal of molecular sciences · 2025Pooled it
- Unveiling Gut Homeostasis Disruption in Sepsis: Towards an Integrated Mechanistic and Translational Roadmap.Cell proliferation · 2026Review
- Factors associated with mortality in older sepsis patients: a nationwide retrospective cohort study in Germany.Age and ageing · 2026Observational
- Epidemiology and outcomes of adult (non-maternity) community-onset sepsis in Ireland: a secondary analysis of acute hospital administrative data 2020-2024.Irish journal of medical science · 2026Article
- Acyl-CoA-binding protein (ACBP): a poor-prognosis biomarker in sepsis and a target for disease mitigation.Signal transduction and targeted therapy · 2026Article
- Mast Cell-Derived CXCL4: A Key Mediator of Ferroptosis and Cardiac Damage in Septic Cardiomyopathy.Immunity, inflammation and disease · 2026Article
- Evaluation of the clinical characteristics and risk factors for in-hospital mortality amongst older persons admitted with bacteraemia in a geriatric ward - a single tertiary centre review.BMC geriatrics · 2026Article
- Biological Age Should Anchor Age-Related Disease Research.Aging and disease · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a systemic inflammatory response triggered by infection that can result in immune regulation disruption and organ dysfunction. As an individual age, a phenomenon known as immunosenescence occurs. Immunosenescence is characterized by the deterioration of immune cells and organs. This decline leads to immune dysfunction, which is closely associated with an increased mortality rate among elderly sepsis patients. Recent studies have revealed that various responses during sepsis can induce premature aging of immune organs and cells in younger individuals, a process referred to as premature immunosenescence, which further accelerates the progression of sepsis and contributes to adverse outcomes. There is a significant correlation between immunosenescence and sepsis; therefore, understanding the specific manifestations and underlying mechanisms of immunosenescence induced by sepsis is imperative. Additionally, treatment strategies aimed at reversing or alleviating both immune aging and immune suppression in septic patients are worthwhile exploring and will also improve understanding of the concept of immunosenescence.
Indexed as
Identifiers
What Socratic 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 Socratic graph.