Evidence map›Paper›PMID 32215570›Full record

ArticleCardiovascular research2021

The effects of sepsis on endothelium and clinical implications.

Elena V Dolmatova, Keke Wang, Rohan Mandavilli, Kathy K Griendling

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed, 1 pooled it
14.7field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

183 citing papers in PubMed, 1 synthesis or guideline pooled it, 289 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Observational
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Observational
  11. Article
  12. TRPV4/IP3R-1-mediated endothelial pyroptosis drives pulmonary microvascular endothelial permeability in endotoxin-induced acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  13. Article
  14. Article
  15. Observational
  16. Review
  17. Article
  18. 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 · 2026
    Review
  19. Review
  20. Article

123 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Elena V DolmatovaDivision of Cardiology, Department of Medicine, Emory University, 101 Woodruff Circle, Atlanta, GA 30322, USA.
Keke WangDivision of Cardiology, Department of Medicine, Emory University, 101 Woodruff Circle, Atlanta, GA 30322, USA.
Rohan MandavilliDivision of Cardiology, Department of Medicine, Emory University, 101 Woodruff Circle, Atlanta, GA 30322, USA.
Kathy K GriendlingDivision of Cardiology, Department of Medicine, Emory University, 101 Woodruff Circle, Atlanta, GA 30322, USA.
Emory University · US

Funding

T cell triggering events and hypertensionP01HL095070 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG · 2009 to 2019
$20.5M
Research Trainng in Academic CardiologyT32HL007745 · NHLBI · EMORY UNIVERSITY · PI TAYLOR, WILLIAM ROBERT · 1994 to 2023
$10.6M
NHLBI NIH HHS P01 HL095070NHLBI NIH HHS T32 HL007745
6 · The paper itself

Abstract

abstractSepsis accounts for nearly 700 000 deaths in Europe annually and is caused by an overwhelming host response to infection resulting in organ failure. The endothelium is an active contributor to sepsis and as such represents a major target for therapy. During sepsis, endothelial cells amplify the immune response and activate the coagulation system. They are both a target and source of inflammation and serve as a link between local and systemic immune responses. In response to cytokines produced by immune cells, the endothelium expresses adhesion molecules and produces vasoactive compounds, inflammatory cytokines, and chemoattractants, thus switching from an anticoagulant to procoagulant state. These responses contribute to local control of infection, but systemic activation can lead to microvascular thrombosis, capillary permeability, hypotension, tissue hypoxia, and ultimately tissue damage. This review focuses on the role of the endothelium in leucocyte adhesion and transmigration as well as production of reactive oxygen and nitrogen species, microRNAs and cytokines, formation of signalling microparticles, and disseminated intravascular coagulation. We also discuss alterations in endothelial permeability and apoptosis. Finally, we review the diagnostic potential of endothelial markers and endothelial pathways as therapeutic targets for this devastating disease.

Indexed as

Blood CoagulationAnimalsAnticoagulantsAnti-Inflammatory AgentsBiomarkersCardiovascular DiseasesEndothelial CellsEndothelium, VascularHumansInflammationInflammation MediatorsSepsisSignal TransductionAnticoagulantsAnti-Inflammatory AgentsBiomarkersInflammation MediatorsDiagnosisEndotheliumMechanismSepsisTreatment

Identifiers

PMID32215570
PMCPMC7810126
OpenAlexW3013230421

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.