Evidence map›Paper›PMID 30986384›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2019

Mechanisms of cardiac collagen deposition in experimental models and human disease.

Randy T Cowling, Daniel Kupsky, Andrew M Kahn, Lori B Daniels, Barry H Greenberg

Open access · greenAbstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 88 citations in OpenAlex.

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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 1 institution in 1 country.

Randy T CowlingDivision of Cardiovascular Medicine, Department of Medicine, University of California, San Diego, California. Electronic address: rcowling@ucsd.edu.
Daniel KupskyDivision of Cardiovascular Medicine, Department of Medicine, University of California, San Diego, California.
Andrew M KahnDivision of Cardiovascular Medicine, Department of Medicine, University of California, San Diego, California.
Lori B DanielsDivision of Cardiovascular Medicine, Department of Medicine, University of California, San Diego, California.
Barry H GreenbergDivision of Cardiovascular Medicine, Department of Medicine, University of California, San Diego, California.
University of California, San Diego · US

Funding

Cardiac fibrosis is regulated by protein turnover in the endoplasmic reticulumR01HL141361 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI COWLING, RANDY T · 2018 to 2021
$1.6M
NHLBI NIH HHS R01 HL141361
6 · The paper itself

Abstract

The inappropriate deposition of extracellular matrix within the heart (termed cardiac fibrosis) is associated with nearly all types of heart disease, including ischemic, hypertensive, diabetic, and valvular. This alteration in the composition of the myocardium can physically limit cardiomyocyte contractility and relaxation, impede electrical conductivity, and hamper regional nutrient diffusion. Fibrosis can be grossly divided into 2 types, namely reparative (where collagen deposition replaces damaged myocardium) and reactive (where typically diffuse collagen deposition occurs without myocardial damage). Despite the widespread association of fibrosis with heart disease and general understanding of its negative impact on heart physiology, it is still not clear when collagen deposition becomes pathologic and translates into disease symptoms. In this review, we have summarized the current knowledge of cardiac fibrosis in human patients and experimental animal models, discussing the mechanisms that have been deduced from the latter in relation to the former. Because assessment of the extent of fibrosis is paramount both as a research tool to further understanding and as a clinical tool to assess patients, we have also summarized the current state of noninvasive/minimally invasive detection systems for cardiac fibrosis. Albeit not exhaustive, our aim is to provide an overview of the current understanding of cardiac fibrosis, both clinically and experimentally.

Indexed as

Disease Models, AnimalAnimalsBiomarkersCollagenFibrosisHeart DiseasesHumansMyocardiumBiomarkersCollagen

Identifiers

PMID30986384
PMCPMC6996650
OpenAlexW2923114894

What OpenQuestion 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 OpenQuestion graph.