Evidence map›Paper›PMID 33339418›Full record

ReviewInternational journal of molecular sciences2020

Small Molecules acting on Myofilaments as Treatments for Heart and Skeletal Muscle Diseases.

Khulud Alsulami, Steven Marston

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.1field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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  8. Review
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  11. Predominant myosin superrelaxed state in canine myocardium with naturally occurring dilated cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2023
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Cardiac myosin filaments are directly regulated by calcium.The Journal of general physiology · 2022
    Article
  18. Article
  19. Review
  20. 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

2 authors at 2 institutions in 2 countries.

Khulud AlsulamiImperial Centre for Translational and Experimental Medicine, Cardiovascular Division, National Heart and Lung Institute, Imperial College London, London W12 0NN, UK.ORCID 0000-0001-5222-5576
Steven MarstonImperial Centre for Translational and Experimental Medicine, Cardiovascular Division, National Heart and Lung Institute, Imperial College London, London W12 0NN, UK.ORCID 0000-0001-6054-6070
Imperial College London · GBKing Abdulaziz City for Science and Technology · SA

Funding

British Heart Foundation RG/11/20/29266
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) are the most prevalent forms of the chronic and progressive pathological condition known as cardiomyopathy. These diseases have different aetiologies; however, they share the feature of haemodynamic abnormalities, which is mainly due to dysfunction in the contractile proteins that make up the contractile unit known as the sarcomere. To date, pharmacological treatment options are not disease-specific and rather focus on managing the symptoms, without addressing the disease mechanism. Earliest attempts at improving cardiac contractility by modulating the sarcomere indirectly (inotropes) resulted in unwanted effects. In contrast, targeting the sarcomere directly, aided by high-throughput screening systems, could identify small molecules with a superior therapeutic value in cardiac muscle disorders. Herein, an extensive literature review of 21 small molecules directed to five different targets was conducted. A simple scoring system was created to assess the suitability of small molecules for therapy by evaluating them in eight different criteria. Most of the compounds failed due to lack of target specificity or poor physicochemical properties. Six compounds stood out, showing a potential therapeutic value in HCM, DCM or heart failure (HF). Omecamtiv Mecarbil and Danicamtiv (myosin activators), Mavacamten, CK-274 and MYK-581 (myosin inhibitors) and AMG 594 (Ca

Indexed as

AnimalsCardiomyopathy, HypertrophicCardiotonic AgentsClinical Trials as TopicHumansMuscle ContractionMuscular DiseasesMyofibrilsCardiotonic Agentscardiomyopathycontractilitycrossbridge cycledrug trialssarcomeretherapeutics

Identifiers

PMID33339418
PMCPMC7767104
OpenAlexW3111237070

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.