Evidence map›Paper›PMID 26125088›Full record

ReviewShock (Augusta, Ga.)2015

ENDOPLASMIC RETICULUM STRESS IN SEPSIS.

Mohammad Moshahid Khan, Weng-Lang Yang, Ping Wang

Abstract readReview
In one paragraph

Review in Shock (Augusta, Ga.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.

  1. Pooled it
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18 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

3 authors at 2 institutions in 1 country.

Mohammad Moshahid Khan*Center for Translational Research, The Feinstein Institute for Medical Research †Department of Surgery, Hofstra North Shore-LIJ School of Medicine, Manhasset, New York.
Weng-Lang Yang
Ping Wang
Hofstra University · USFeinstein 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
NIGMS NIH HHS R01 GM053008NIGMS NIH HHS R01GM053008NIGMS NIH HHS R01 GM057468NIGMS NIH HHS R01GM057468
6 · The paper itself

Abstract

Sepsis is an enormous public health issue and the leading cause of death in critically ill patients in intensive care units. Overwhelming inflammation, characterized by cytokine storm, oxidative threats, and neutrophil sequestration, is an underlying component of sepsis-associated organ failure. Despite recent advances in sepsis research, there is still no effective treatment available beyond the standard of care and supportive therapy. To reduce sepsis-related mortality, a better understanding of the biological mechanism associated with sepsis is essential. Endoplasmic reticulum (ER), a subcellular organelle, is responsible for the facilitation of protein folding and assembly and involved in several other physiological activities. Under stress and inflammatory conditions, ER loses homeostasis in its function, which is termed ER stress. During ER stress, unfolded protein response (UPR) is activated to restore ER function to its normal balance. However, once stress is beyond the compensatory capacity of UPR or protracted, apoptosis would be initiated by triggering cell injuries, even cell death. As such, ER stress and UPR are reported to be implicated in several pathological and inflammatory conditions. Although the detrimental role of ER stress during infections has been demonstrated, there is growing evidence that ER stress participates in the pathogenesis of sepsis. In this review, we summarize current research in the context of ER stress and UPR signaling associated with sepsis and its related clinical conditions, such as trauma-hemorrhage and ischemia/reperfusion injury. We also discuss the potential implications of ER stress as a novel therapeutic target and prognostic marker in patients with sepsis.

Indexed as

Activating Transcription Factor 6ApoptosiseIF-2 KinaseEndoplasmic Reticulum StressHumansInflammationReperfusion InjurySepsisShock, HemorrhagicSignal TransductionStress, PhysiologicalUnfolded Protein ResponseActivating Transcription Factor 6ATF6 protein, humanEIF2AK3 protein, humaneIF-2 Kinase

Identifiers

PMID26125088
PMCPMC4575622
OpenAlexW2418662167

What OpenQuestion holds

Textmetadata
LicenceTDM
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.