Evidence map›Paper›PMID 35259455›Full record

ReviewCellular signalling2022

Friend or foe? Unraveling the complex roles of protein tyrosine phosphatases in cardiac disease and development.

Maike Krenz

Open access · greenAbstract readReview
In one paragraph

Review in Cellular signalling, 2022. 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
0.3field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Review
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

1 author at 1 institution in 1 country.

Maike KrenzDalton Cardiovascular Research Center and Department of Medical Pharmacology & Physiology, School of Medicine, University of Missouri, USA. Electronic address: krenzm@missouri.edu.
University of Missouri · US

Funding

SHP2 controls cardiac stress adaptationR01HL116525 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI KRENZ, MAIKE · 2013 to 2016
$1.4M
NHLBI NIH HHS R01 HL116525
6 · The paper itself

Abstract

Regulation of protein tyrosine phosphorylation is critical for most, if not all, fundamental cellular processes. However, we still do not fully understand the complex and tissue-specific roles of protein tyrosine phosphatases in the normal heart or in cardiac pathology. This review compares and contrasts the various roles of protein tyrosine phosphatases known to date in the context of cardiac disease and development. In particular, it will be considered how specific protein tyrosine phosphatases control cardiac hypertrophy and cardiomyocyte contractility, how protein tyrosine phosphatases contribute to or ameliorate injury induced by ischaemia / reperfusion or hypoxia / reoxygenation, and how protein tyrosine phosphatases are involved in normal heart development and congenital heart disease. This review delves into the newest developments and current challenges in the field, and highlights knowledge gaps and emerging opportunities for future research.

Indexed as

Heart DiseasesProtein Tyrosine PhosphatasesHumansMyocytes, CardiacPhosphorylationProtein Tyrosine PhosphatasesCardiac developmentCongenital heart diseaseHeart failureIschaemia / reperfusionProtein tyrosine phosphataseSignalling

Identifiers

PMID35259455
PMCPMC9038168
OpenAlexW4220752831

What Socratic 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 Socratic graph.