Evidence map›Paper›PMID 27252164›Full record

ReviewPhysiology (Bethesda, Md.)2016

Viewing Extrinsic Proteotoxic Stress Through the Lens of Amyloid Cardiomyopathy.

Valerie Sapp, Mohit Jain, Ronglih Liao

Abstract readReview
In one paragraph

Review in Physiology (Bethesda, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Cu(II) Binding Increases the Soluble Toxicity of Amyloidogenic Light Chains.International journal of molecular sciences · 2022
    Article
  5. Review
  6. Article
  7. Article
  8. 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

3 authors.

Valerie SappDepartments of Medicine & Pharmacology, University of California San Diego, San Diego, California; and.
Mohit JainDepartments of Medicine & Pharmacology, University of California San Diego, San Diego, California; and.
Ronglih LiaoDivision of Genetics and Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.

Funding

GRADUATE TRAINING IN CELLULAR &MOLECULAR PHARMACOLOGYT32GM007752 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROWN, JOAN HELLER, HANDEL, TRACY M · 1985 to 2023
$13.5M
Molecular Mechanisms and Treatment of Primary Amyloid AL CardiomyopathyR01HL088533 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIAO, RONGLIH · 2007 to 2015
$4.3M
Metabolic underpinnings of AL amyloid cardiomyopathyR01HL128135 · NHLBI · STANFORD UNIVERSITY · PI LIAO, RONGLIH · 2015 to 2018
$2.5M
A systems approach to metabolic dysregulation in the heartK08HL107451 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI JAIN, MOHIT · 2011 to 2015
$685k
NHLBI NIH HHS K08 HL107451NHLBI NIH HHS R01 HL088533NHLBI NIH HHS R01 HL128135NIGMS NIH HHS T32 GM007752
6 · The paper itself

Abstract

Proteotoxicity refers to toxic stress caused by misfolded proteins of extrinsic or intrinsic origin and plays an integral role in the pathogenesis of cardiovascular diseases. Herein, we provide an overview of the current understanding of mechanisms underlying proteotoxicity and its contribution in the pathogenesis of amyloid cardiomyopathy.

Indexed as

Stress, PhysiologicalAmyloidogenic ProteinsAnimalsCardiomyopathiesHumansProteostasis DeficienciesAmyloidogenic Proteins

Identifiers

PMID27252164
PMCPMC6195664

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.