Evidence mapPaperPMID 32197794Full record

ReviewPharmacology & therapeutics2020

Targeting of G-protein coupled receptors in sepsis.

Abdul Rehman, Noor Ul-Ain Baloch, John P Morrow, Pál Pacher, György Haskó

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Effect of premorbid beta-blockers on cardiac function and clinical outcomes in septic patients: a retrospective study.Journal of critical care medicine (Universitatea de Medicina si Farmacie din Targu-Mures) · 2026
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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 4 institutions in 1 country.

Abdul RehmanDepartment of Medicine, Rutgers-New Jersey Medical School, Newark, NJ, United States.
Noor Ul-Ain BalochDepartment of Medicine, Rutgers-New Jersey Medical School, Newark, NJ, United States.
John P MorrowDepartment of Medicine, Columbia University, New York City, NY, United States.
Pál PacherLaboratory of Cardiovascular Physiology and Tissue Injury, National Institutes of Health, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, United States.
György HaskóDepartment of Anesthesiology, Columbia University, New York City, NY, United States. Electronic address: gh2503@cumc.columbia.edu.
Columbia University · USNational Institute on Alcohol Abuse and Alcoholism · USRutgers New Jersey Medical SchoolRutgers, The State University of New Jersey · US

Funding

Mechanism of oxidative/nitrosative stress and inflammation-induced tissue injuryZIAAA000375 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI PACHER, PAL · 2009 to 2025
$27.8M
Purinergic signaling in trauma and sepsisR01GM066189 · NIGMS · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI HASKO, GEORGE · 2002 to 2020
$4.7M
Purinergic signaling in granuloma-forming Th2 immunityR01DK113790 · NIDDK · RBHS-NEW JERSEY MEDICAL SCHOOL · PI GAUSE, WILLIAM CLARK, HASKO, GEORGE · 2017 to 2020
$1.9M
NIDDK NIH HHS R01 DK113790NIGMS NIH HHS R01 GM066189
6 · The paper itself

Abstract

The Third International Consensus Definitions (Sepsis-3) define sepsis as life-threatening multi-organ dysfunction caused by a dysregulated host response to infection. Sepsis can progress to septic shock-an even more lethal condition associated with profound circulatory, cellular and metabolic abnormalities. Septic shock remains a leading cause of death in intensive care units and carries a mortality of almost 25%. Despite significant advances in our understanding of the pathobiology of sepsis, therapeutic interventions have not translated into tangible differences in the overall outcome for patients. Clinical trials of antagonists of various pro-inflammatory mediators in sepsis have been largely unsuccessful in the past. Given the diverse physiologic roles played by G-protein coupled receptors (GPCR), modulation of GPCR signaling for the treatment of sepsis has also been explored. Traditional pharmacologic approaches have mainly focused on ligands targeting the extracellular domains of GPCR. However, novel techniques aimed at modulating GPCR intracellularly through aptamers, pepducins and intrabodies have opened a fresh avenue of therapeutic possibilities. In this review, we summarize the diverse roles played by various subfamilies of GPCR in the pathogenesis of sepsis and identify potential targets for pharmacotherapy through these novel approaches.

Indexed as

AnimalsDrug DevelopmentHumansLigandsMolecular Targeted TherapyReceptors, G-Protein-CoupledSepsisShock, SepticSignal TransductionLigandsReceptors, G-Protein-CoupledAptamersG-protein coupled receptorsIntrabodiesPepducinsSepsisSeptic shock

Identifiers

PMID32197794
PMCPMC7388546
OpenAlexW3010924801

What Socratic 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 Socratic graph.