Evidence mapPaperPMID 25320235Full record

Trial reportScience translational medicine2014

PCSK9 is a critical regulator of the innate immune response and septic shock outcome.

Keith R Walley, Katherine R Thain, James A Russell, Muredach P Reilly, Nuala J Meyer, Jane F Ferguson, Jason D Christie, Taka-aki Nakada, Chris D Fjell, Simone A Thair and 2 more

2 registry-linked trialsAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Science translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 192 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed, 3 pooled it
24.6field-weighted citation impact, top 1% 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.

NCT03634293 phase2 / phase3unknown statusnot on this mapstarted 2019, after this paper: background citation

PCSK9 Inhibitor: a New Tool to Fight Septic Shock

TypeinterventionalSponsorWolfson Medical CenterRan2019 to 2021Enrolled712ConditionsSepsis, Septic ShockArmsAlirocumab Injectable Product, Saline Solution
NCT03869073 phase2unknown statusnot on this mapstarted 2019, after this paper: background citation

Randomized, Double-blind, Placebo-controlled Phase 2a Trial of Efficacy and Safety of Evolocumab for PCSK9 Lowering in Early Acute Sepsis

TypeinterventionalSponsorUniversity of British ColumbiaRan2019 to 2021Enrolled36ConditionsSepsisArmsEvolocumab, Placebo
3 · Its place in the literature

Who cites it

192 citing papers in PubMed, 3 syntheses or guidelines pooled it, 367 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Pooled it
  4. Trial
  5. PCSK9 Inhibition During the Inflammatory Stage of SARS-CoV-2 Infection.Journal of the American College of Cardiology · 2023
    Trial
  6. Trial
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  8. Trial
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  10. Review
  11. Article
  12. PCSK9 in critical illness - It's not all about lipids.Annals of clinical biochemistry · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

132 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Keith R WalleyCentre for Heart Lung Innovation, University of British Columbia, Vancouver V6Z 1Y6, Canada. keith.walley@hli.ubc.ca.
Katherine R ThainCentre for Heart Lung Innovation, University of British Columbia, Vancouver V6Z 1Y6, Canada.
James A RussellCentre for Heart Lung Innovation, University of British Columbia, Vancouver V6Z 1Y6, Canada.
Muredach P ReillyCardiovascular Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.
Nuala J MeyerPulmonary, Allergy, and Critical Care Division, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Translational Lung Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.
Jane F FergusonCardiovascular Institute, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.
Jason D ChristiePulmonary, Allergy, and Critical Care Division, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Translational Lung Biology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.
Taka-aki NakadaDepartment of Emergency and Critical Care Medicine, Chiba University Graduate School of Medicine, Chiba 260-8677, Japan.
Chris D FjellCentre for Heart Lung Innovation, University of British Columbia, Vancouver V6Z 1Y6, Canada.
Simone A ThairCentre for Heart Lung Innovation, University of British Columbia, Vancouver V6Z 1Y6, Canada.
Mihai S CirsteaCentre for Heart Lung Innovation, University of British Columbia, Vancouver V6Z 1Y6, Canada.
John H BoydCentre for Heart Lung Innovation, University of British Columbia, Vancouver V6Z 1Y6, Canada.
University of Pennsylvania · USChiba University · JP

Funding

CIHRNCATS NIH HHS UL1 TR000003NCATS NIH HHS UL1TR000003NHLBI NIH HHS K24 HL107643NHLBI NIH HHS P50 HL083799NHLBI NIH HHS P50-HL-083799NHLBI NIH HHS R01 HL113147
6 · The paper itself

Abstract

A decrease in the activity of proprotein convertase subtilisin/kexin type 9 (PCSK9) increases the amount of low-density lipoprotein (LDL) receptors on liver cells and, therefore, LDL clearance. The clearance of lipids from pathogens is related to endogenous lipid clearance; thus, PCSK9 may also regulate removal of pathogen lipids such as lipopolysaccharide (LPS). Compared to controls, Pcsk9 knockout mice displayed decreases in inflammatory cytokine production and in other physiological responses to LPS. In human liver cells, PCSK9 inhibited LPS uptake, a necessary step in systemic clearance and detoxification. Pharmacological inhibition of PCSK9 improved survival and inflammation in murine polymicrobial peritonitis. Human PCSK9 loss-of-function genetic variants were associated with improved survival in septic shock patients and a decrease in inflammatory cytokine response both in septic shock patients and in healthy volunteers after LPS administration. The PCSK9 effect was abrogated in LDL receptor (LDLR) knockout mice and in humans who are homozygous for an LDLR variant that is resistant to PCSK9. Together, our results show that reduced PCSK9 function is associated with increased pathogen lipid clearance via the LDLR, a decreased inflammatory response, and improved septic shock outcome.

Indexed as

Immunity, InnateAnimalsDisease Models, AnimalGenetic VariationHep G2 CellsHumansLipopolysaccharidesMaleMice, Inbred C57BLMice, KnockoutProprotein Convertase 9Proprotein ConvertasesSerine EndopeptidasesShock, SepticLipopolysaccharidesPCSK9 protein, humanPcsk9 protein, mouseProprotein Convertase 9Proprotein ConvertasesSerine Endopeptidases

Identifiers

PMID25320235
PMCPMC4342147
OpenAlexW1990237691

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.