Evidence map›Paper›PMID 23136259›Full record

ReviewJournal of leukocyte biology2013

Current trends in inflammatory and immunomodulatory mediators in sepsis.

Monowar Aziz, Asha Jacob, Weng-Lang Yang, Akihisa Matsuda, Ping Wang

Open access · greenAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

173 citing papers in PubMed, 309 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Edaravone's reno-protective effects against chronic heat-stress exposure.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Article
  7. Article
  8. Article
  9. Observational
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Profiling Molecular Changes of Host Response to Predict Outcome in Children with Septic Shock.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2024
    Article
  17. Article
  18. Article
  19. Article
  20. Article

113 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

5 authors at 1 institution in 1 country.

Monowar AzizCenter for Immunology and Inflammation, The Feinstein Institute for Medical Research, Hofstra North Shore-LIJ School of Medicine, 350 Community Dr., Manhasset, NY 11030, USA.
Asha Jacob
Weng-Lang Yang
Akihisa Matsuda
Ping Wang
Feinstein Institute for Medical Research · US

Funding

SEPSIS--MEDIATORS AND CARDIOVASCULAR RESPONSESR01GM057468 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, PING · 1998 to 2015
$3.8M
Modulation of Hepatocellular Function in SepsisR01GM053008 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WANG, PING · 2001 to 2015
$3.7M
Radiation Combined Injury: Mechanisms and Therapeutic ApproachesR33AI080536 · NIAID · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI WANG, PING · 2010 to 2012
$1.3M
NIAID NIH HHS R33 AI 080536NIAID NIH HHS R33 AI080536NIGMS NIH HHS R01 GM053008NIGMS NIH HHS R01 GM057468
6 · The paper itself

Abstract

Sepsis refers to severe systemic inflammation in response to invading pathogens. An overwhelming immune response, as mediated by the release of various inflammatory mediators, can lead to shock, multiple organ damage, and even death. Cytokines, proteases, lipid mediators, gaseous substances, vasoactive peptides, and cell stress markers play key roles in sepsis pathophysiology. Various adhesion molecules and chemokines sequester and activate neutrophils into the target organs, further augmenting inflammation and tissue damage. Although the anti-inflammatory substances counterbalance proinflammatory mediators, prolonged immune modulation may cause host susceptibility to concurrent infections, thus reflecting enormous challenge toward developing effective clinical therapy against sepsis. To understand the complex interplay between pro- and anti-inflammatory phenomenon in sepsis, there is still an unmet need to study newly characterized mediators. In addition, revealing the current trends of novel mediators will upgrade our understanding on their signal transduction, cross-talk, and synergistic and immunomodulating roles during sepsis. This review highlights the latest discoveries of the mediators in sepsis linking to innate and adaptive immune systems, which may lead to resolution of many unexplored queries.

Indexed as

Adaptive ImmunityAnimalsChemokinesHumansImmunity, InnateImmunologic FactorsInfectionsInflammationInflammation MediatorsNeutrophil ActivationNeutrophilsSepsisChemokinesImmunologic FactorsInflammation Mediators

Identifiers

PMID23136259
PMCPMC3579020
OpenAlexW2160167304

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.