ReviewJournal of medical genetics2016
Novel myosin-based therapies for congenital cardiac and skeletal myopathies.
Review in Journal of medical genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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.
Who cites it
7 citing papers in PubMed.
- Article
- Virus-free transfection, transient expression, and purification of human cardiac myosin in mammalian muscle cells for biochemical and biophysical assays.Scientific reports · 2023Article
- Comparative study of binding pocket structure and dynamics in cardiac and skeletal myosin.Biophysical journal · 2023Article
- Hypertrophic cardiomyopathy disease results from disparate impairments of cardiac myosin function and auto-inhibition.Nature communications · 2018Article
- Blebbistatin Effects Expose Hidden Secrets in the Force-Generating Cycle of Actin and Myosin.Biophysical journal · 2018Article
- Do Actomyosin Single-Molecule Mechanics Data Predict Mechanics of Contracting Muscle?International journal of molecular sciences · 2018Review
- Allosteric modulation of cardiac myosin dynamics by omecamtiv mecarbil.PLoS computational biology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The dysfunction in a number of inherited cardiac and skeletal myopathies is primarily due to an altered ability of myofilaments to generate force and motion. Despite this crucial knowledge, there are, currently, no effective therapeutic interventions for these diseases. In this short review, we discuss recent findings giving strong evidence that genetically or pharmacologically modulating one of the myofilament proteins, myosin, could alleviate the muscle pathology. This should constitute a research and clinical priority.
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Registered trials
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.