Evidence map›Paper›PMID 27768389›Full record

ArticleAmerican journal of respiratory and critical care medicine2017

A Missense Genetic Variant in LRRC16A/CARMIL1 Improves Acute Respiratory Distress Syndrome Survival by Attenuating Platelet Count Decline.

Yongyue Wei, Paula Tejera, Zhaoxi Wang, Ruyang Zhang, Feng Chen, Li Su, Xihong Lin, Ednan K Bajwa, B Taylor Thompson, David C Christiani

Abstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Article
  4. Article
  5. Integrative omics and multi-cohort identifyJournal of biomedical research · 2025
    Article
  6. Article
  7. American journal of respiratory cell and molecular biology · 2023
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Platelet Biogenesis in the Lung Circulation.Physiology (Bethesda, Md.) · 2019
    Review
  17. Review
  18. Article
  19. Observational
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Yongyue Wei1 Department of Environmental Health and.
Paula Tejera1 Department of Environmental Health and.
Zhaoxi Wang1 Department of Environmental Health and.
Ruyang Zhang1 Department of Environmental Health and.
Feng Chen2 Department of Biostatistics, School of Public Health and.
Li Su1 Department of Environmental Health and.
Xihong Lin4 Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts.
Ednan K Bajwa5 Division of Pulmonary and Critical Care, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
B Taylor Thompson5 Division of Pulmonary and Critical Care, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
David C Christiani1 Department of Environmental Health and.
Harvard University · USNanjing Medical University · CN

Funding

MOLECULAR EPIDEMIOLOGY OF ARDSR01HL060710 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI CHRISTIANI, DAVID C · 2000 to 2015
$8.4M
NHLBI NIH HHS R01 HL060710
6 · The paper itself

Abstract

rationalePlatelets are believed to contribute to acute respiratory distress syndrome (ARDS) pathogenesis through inflammatory coagulation pathways. We recently reported that leucine-rich repeat-containing 16A (LRRC16A) modulates baseline platelet counts to mediate ARDS risk.

objectivesTo examine the role of LRRC16A in ARDS survival and its mediating effect through platelets.

methodsA total of 414 cases with ARDS from intensive care units (ICUs) were recruited who had exome-wide genotyping data, detailed platelet counts, and follow-up data during ICU hospitalization. Association of LRRC16A single-nucleotide polymorphisms (SNPs) and ARDS prognosis, and the mediating effect of SNPs through platelet counts were analyzed. LRRC16A mRNA expression levels for 39 cases with ARDS were also evaluated. MEASUREMENTS AND MAIN

resultsMissense SNP rs9358856G>A within LRRC16A was associated with favorable survival within 28 days (hazard ratio [HR], 0.57; 95% confidence interval [CI], 0.38-0.87; P = 0.0084) and 60 days (P = 0.0021) after ICU admission. Patients with ARDS who carried the variant genotype versus the wild-type genotype showed an attenuated platelet count decline (∆PLT) within 28 days (difference of ∆PLT, -27.8; P = 0.025) after ICU admission. Patients with ∆PLT were associated with favorable ARDS outcomes. Mediation analysis indicated that the SNP prognostic effect was mediated through ∆PLT within 28 days (28-day survival: HR

conclusionsLRRC16A appears to mediate ∆PLT after ICU admission to affect the prognosis in patients with ARDS.

Indexed as

AgedFemaleGenetic VariationHumansMaleMicrofilament ProteinsMiddle AgedMutation, MissensePlatelet CountPolymorphism, Single NucleotideProportional Hazards ModelsRespiratory Distress SyndromeRisk FactorsCARMIL1 protein, humanMicrofilament ProteinsARDS outcomecausal mediation analysisplateletsSNP

Identifiers

PMID27768389
PMCPMC5443896
OpenAlexW2538193286

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.