Evidence map›Paper›PMID 28577155›Full record

ReviewBiophysical reviews2018

RBM20, a potential target for treatment of cardiomyopathy via titin isoform switching.

Wei Guo, Mingming Sun

Open access · bronzeAbstract readReview
In one paragraph

Review in Biophysical reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Mechanisms of RBM20 Cardiomyopathy: Insights From Model Systems.Circulation. Genomic and precision medicine · 2024
    Review
  4. Titin: roles in cardiac function and diseases.Frontiers in physiology · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. RBM20, a Therapeutic Target to Alleviate Myocardial StiffnessFrontiers in cardiovascular medicine · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Angiotensin II Influences Pre-mRNA Splicing Regulation by EnhancingInternational journal of molecular sciences · 2019
    Article
  18. Article
  19. Alternative splicing in cardiomyopathy.Biophysical reviews · 2018
    Review
  20. 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

2 authors at 1 institution in 1 country.

Wei GuoAnimal Science, University of Wyoming, Laramie, WY, 82071, USA. wguo3@uwyo.edu.ORCID http://orcid.org/0000-0002-9158-8107
Mingming SunAnimal Science, University of Wyoming, Laramie, WY, 82071, USA.
University of Wyoming · US

Funding

Wyoming INBRE Phase 4- Equipment Supplement for x-ray diffractometer for Center for Advanced Scientific InstrumentationP20GM103432 · NIGMS · UNIVERSITY OF WYOMING · PI Robert Scott Seville · 2012 to 2026
$56.8M
American Heart Association 16BGIA27790136National Institute of Food and Agriculture 1009266NIGMS NIH HHS NIGMSP20GM103432
6 · The paper itself

Abstract

Cardiomyopathy, also known as heart muscle disease, is an unfavorable condition leading to alterations in myocardial contraction and/or impaired ability of ventricular filling. The onset and development of cardiomyopathy have not currently been well defined. Titin is a giant multifunctional sarcomeric filament protein that provides passive stiffness to cardiomyocytes and has been implicated to play an important role in the origin and development of cardiomyopathy and heart failure. Titin-based passive stiffness can be mainly adjusted by isoform switching and post-translational modifications in the spring regions. Recently, genetic mutations of TTN have been identified that can also contribute to variable passive stiffness, though the detailed mechanisms remain unclear. In this review, we will discuss titin isoform switching as it relates to alternative splicing during development stages and differences between species and muscle types. We provide an update on the regulatory mechanisms of TTN splicing controlled by RBM20 and cover the roles of TTN splicing in adjusting the diastolic stiffness and systolic compliance of the healthy and the failing heart. Finally, this review attempts to provide future directions for RBM20 as a potential target for pharmacological intervention in cardiomyopathy and heart failure.

Indexed as

Alternative splicingCardiomyopathyRBM20Titin isoform switching

Identifiers

PMID28577155
PMCPMC5803173
OpenAlexW2620921528

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.