ReviewJournal of inflammation research2024
Sepsis-Induced Endothelial Dysfunction: Permeability and Regulated Cell Death.
Review in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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
24 citing papers in PubMed.
- Attenuation of sepsis-associated acute lung injury by lncRNA LINC00052 via sponging miR-106b-5p.Journal of cardiothoracic surgery · 2026Article
- Targeted silencing of CLYBL with platelet-mimetic siRNA nanoparticles drives itaconate-mediated macrophage reprogramming and protects against sepsis-triggered lung cell death.Cell death discovery · 2026Article
- From Glycocalyx Shedding to Microvascular Collapse in Sepsis: Endothelial Pathophysiology, Organ Dysfunction, and Mechanistic Biomarkers.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Targeting the TLR4/NF-κB/TNF-α/MMP axis with dexamethasone attenuates glycocalyx degradation and restores microcirculatory perfusion in septic kidneys.Scientific reports · 2026Article
- Organ-specific inflammatory profiles during sepsis: divergent macrophage polarization and oxidative stress response in lung and liver in mouse model of caecal ligation and puncture.Journal of inflammation (London, England) · 2026Article
- Article
- Advanced Age in Mice Exacerbates Sepsis-Induced Inflammation, Vascular Permeability, and Multi-Organ Dysfunction.Shock (Augusta, Ga.) · 2026Article
- Dipeptidase-1 Contributes to Sepsis-Associated Endothelial Dysfunction via the EGR1/NF-κB Signaling Axis.International journal of general medicine · 2026Article
- Regulation of histones in thromboinflammation.Frontiers in immunology · 2026Review
- Burns: The "Fuse" That Ignites Organ Crisis - A Narrative Review of Mechanisms and Crosstalk in Post-Burn MODS.Journal of inflammation research · 2026Review
- S100A12 drives inflammatory and metabolic reprogramming in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2026Review
- The role of programmed cell death in chronic obstructive pulmonary disease: from pathogenesis to treatment.Frontiers in immunology · 2026Review
- Angiopoietin-2 Surpasses Soluble Thrombomodulin and Syndecan-1 in Characterizing Septic Shock and Predicting Mortality--A Prospective Observational Study.Journal of inflammation research · 2026Article
- IL-1βCell death discovery · 2025Article
- PD-L1Respiratory research · 2025Article
- Research advances on the role of programmed endothelial cell death in sepsis.Cell death discovery · 2025Review
- Immunodynamic Disruption in Sepsis: Mechanisms and Strategies for Personalized Immunomodulation.Biomedicines · 2025Review
- Current Insights into Glutathione Depletion in Adult Septic Patients.Antioxidants (Basel, Switzerland) · 2025Review
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- Sepsis-Induced Endothelial Barrier Dysfunction: Mechanisms, Pathology, and Therapeutic Advances.Research (Washington, D.C.) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Endothelial cells (ECs) are an important cell type typically affected in sepsis, resulting in compromised barrier function and various forms of regulated cell death (RCD). However, the precise mechanisms underlying sepsis-induced EC damage remain unclear. This review summarizes the recent research progress on factors and mechanisms that may affect the permeability and RCD of ECs under septic conditions, including glycocalyx, damage-associated molecular patterns, and various forms of RCD in ECs, such as apoptosis, pyroptosis, ferroptosis, and autophagy. This review offers important insights into the underlying mechanisms of endothelial dysfunction in sepsis, aiming to contribute to developing small-molecule targeted clinical therapies.
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.