Evidence map›Paper›PMID 29956071›Full record

ArticleInflammation2018

PI3K/AKT and CD40L Signaling Regulate Platelet Activation and Endothelial Cell Damage in Sepsis.

Peng Wan, Xiang Tan, Yan Xiang, Huasheng Tong, Min Yu

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Early Platelet Dysfunction in Sepsis: An ICU Pilot Study.Pathogens (Basel, Switzerland) · 2026
    Observational
  2. Review
  3. Review
  4. Article
  5. ADAM10-a "multitasker" in sepsis: focus on its posttranslational target.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Frontiers in pharmacology · 2020
    Article
  13. Article
  14. Article
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

5 authors at 1 institution in 1 country.

Peng WanDepartment of Critical Care Medicine, the People's Hospital of China Three Gorges University, Yichang, 443110, Hubei, China.
Xiang TanDepartment of Critical Care Medicine, the People's Hospital of China Three Gorges University, Yichang, 443110, Hubei, China.
Yan XiangDepartment of Critical Care Medicine, the People's Hospital of China Three Gorges University, Yichang, 443110, Hubei, China.
Huasheng TongDepartment of Critical Care Medicine, the People's Hospital of China Three Gorges University, Yichang, 443110, Hubei, China.
Min YuDepartment of Critical Care Medicine, the People's Hospital of China Three Gorges University, Yichang, 443110, Hubei, China. Yuminicu@163.com.
China Three Gorges University · CN

Funding

Chinese National Natural Science Foundation 81471839Chinese National Natural Science Foundation 81501045Natural Science Foundation of Yichang of Hubei Province of China A16-301-13
6 · The paper itself

Abstract

Platelets contribute to inflammation and their activation has been suggested as versatile effectors of sepsis. Activation of platelets promotes secretion of CD40L that induces sepsis and multiple organ dysfunction syndrome (MODS). However, the mechanisms regulate platelet-derived CD40L are not fully understood. Activation of PI3K/Akt pathway has been reported as a key component of sepsis, whereas the role of PI3K/Akt pathway in platelet-derived CD40L is unknown. In this study, we identified PI3K/Akt pathway as a key regulator of CD40L secretion by platelets. Significantly, inhibition of PI3K/Akt pathway by Ly294002 attenuated platelet activation and CD40L production. Moreover, PI3K/Akt pathway blocking suppresses vascular endothelial cells in vivo. Furthermore, the expression of biomarkers that represent the severity of sepsis, such as ICAM-1, VCAM-1, and E-selectin, was also suppressed by Ly294002. Altogether, our results confirm the pivotal role of PI3K/Akt pathway in sepsis and its inhibition might be a potential therapeutic target.

Indexed as

Platelet ActivationSignal TransductionAnimalsCD40 LigandChromonesEndothelial CellsHumansMetabolic Networks and PathwaysMorpholinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSepsis2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneCD40 LigandChromonesMorpholinesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCD40LPI3K/Akt pathwayplatelet activationsepsis

Identifiers

PMID29956071
OpenAlexW2810171846

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.