Evidence map›Paper›PMID 25277298›Full record

ReviewJournal of cardiovascular translational research2014

The role of intrinsic apoptotic signaling in hemorrhagic shock-induced microvascular endothelial cell barrier dysfunction.

Devendra A Sawant, Binu Tharakan, Felicia A Hunter, Ed W Childs

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of cardiovascular translational research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  5. Review
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  12. Ulinastatin mediates protection against vascular hyperpermeability following hemorrhagic shock.International journal of clinical and experimental pathology · 2015
    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

4 authors at 2 institutions in 1 country.

Devendra A SawantDepartment of Surgery, Morehouse School of Medicine, 720 Westview Drive SW, Atlanta, GA, 30310, USA.
Binu Tharakan
Felicia A Hunter
Ed W Childs
Morehouse School of Medicine · USTexas A&M Health Science Center · US

Funding

NHLBI NIH HHS 1K01HL07815-01A1
6 · The paper itself

Abstract

Hemorrhagic shock leads to endothelial cell barrier dysfunction resulting in microvascular hyperpermeability. Hemorrhagic shock-induced microvascular hyperpermeability is associated with worse clinical outcomes in patients with traumatic injuries. The results from our laboratory have illustrated a possible pathophysiological mechanism showing involvement of mitochondria-mediated "intrinsic" apoptotic signaling in regulating hemorrhagic shock-induced microvascular hyperpermeability. Hemorrhagic shock results in overexpression of Bcl-2 family of pro-apoptotic protein, BAK, in the microvascular endothelial cells. The increase in BAK initiates "intrinsic" apoptotic signaling cascade with the release of mitochondrial cytochrome c in the cytoplasm and activation of downstream effector caspase-3, leading to loss of endothelial cell barrier integrity. Thus, this review article offers a brief overview of important findings from our past and present research work along with new leads for future research. The summary of our research work will provide information leading to different avenues in developing novel strategies against microvascular hyperpermeability following hemorrhagic shock.

Indexed as

ApoptosisCapillary PermeabilityAnimalsApoptosis Regulatory ProteinsCardiovascular AgentsDrug DesignEndothelium, VascularHumansMicrovesselsMitochondriaMolecular Targeted TherapyShock, HemorrhagicSignal TransductionApoptosis Regulatory ProteinsCardiovascular Agents

Identifiers

PMID25277298
OpenAlexW2064051725

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.