Evidence map›Paper›PMID 29457788›Full record

ArticleThe Journal of clinical investigation2018

SCN5A: the greatest HITS collection.

David S Park, Glenn I Fishman

Abstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

David S Park
Glenn I Fishman

Funding

Purkinje Cells and Arrhythmia MechanismsR01HL105983 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHMAN, GLENN I · 2011 to 2019
$5.2M
Etv1 is an Essential Regulator of Fast Conduction Tissues in the HeartR01HL132073 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI PARK, DAVID S · 2017 to 2021
$2.1M
NHLBI NIH HHS R01 HL105983NHLBI NIH HHS R01 HL132073
6 · The paper itself

Abstract

Heart failure (HF) has been referred to as the cardiovascular epidemic of our time. Understanding the molecular determinants of HF disease progression and mortality risk is of utmost importance. In this issue of the JCI, Zhang et al. uncover an important link between clinical HF mortality risk and a common variant that regulates SCN5A expression through microRNA-dependent (miR-dependent)mechanisms. They also demonstrate that haploinsufficiency of SCN5A is associated with increased accumulation of reactive oxygen species (ROS) in a genetically engineered murine model. Their data suggest that even modest depression of SCN5A expression may promote pathologic cardiac remodeling and progression of HF.

Indexed as

Heart FailureMicroRNAsAnimalsHeartMiceNAV1.5 Voltage-Gated Sodium ChannelMicroRNAsNAV1.5 Voltage-Gated Sodium ChannelSCN5A protein, humanScn5a protein, mouse

Identifiers

PMID29457788
PMCPMC5824860

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.