ReviewJournal of muscle research and cell motility2017
When signalling goes wrong: pathogenic variants in structural and signalling proteins causing cardiomyopathies.
Review in Journal of muscle research and cell motility, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 15 citations in OpenAlex.
- Epigenetics, Modifiers, and Molecular Noise: Rethinking Pathophysiology in Dilated and Hypertrophic Cardiomyopathies.International journal of molecular sciences · 2026Review
- Hypertrophic Cardiomyopathy: Current Perspectives.Reviews in cardiovascular medicine · 2025Review
- Structural and signaling proteins in the Z-disk and their role in cardiomyopathies.Frontiers in physiology · 2023Review
- Cardiovascular Involvement in PediatricJournal of cardiovascular development and disease · 2022Article
- Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022Review
- The p.Ala2430Val mutation in filamin C causes a "hypertrophic myofibrillar cardiomyopathy".Journal of muscle research and cell motility · 2021Article
- Homozygous expression of the myofibrillar myopathy-associated p.W2710X filamin C variant reveals major pathomechanisms of sarcomeric lesion formation.Acta neuropathologica communications · 2020Article
- Histopathology in HCM.Global cardiology science & practice · 2018Review
- Four and a half LIM domain protein signaling and cardiomyopathy.Biophysical reviews · 2018Review
- Aberrant Protein Turn-Over Associated With Myofibrillar Disorganization in FHL1 Knockout Mice.Frontiers in genetics · 2018Article
- Proteomic Identification of Heat Shock-Induced Danger Signals in a Melanoma Cell Lysate Used in Dendritic Cell-Based Cancer Immunotherapy.Journal of immunology research · 2018Article
- Editorial on EMC 2017 special issue.Journal of muscle research and cell motility · 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Cardiomyopathies are a diverse group of cardiac disorders with distinct phenotypes, depending on the proteins and pathways affected. A substantial proportion of cardiomyopathies are inherited and those will be the focus of this review article. With the wide application of high-throughput sequencing in the practice of clinical genetics, the roles of novel genes in cardiomyopathies are recognised. Here, we focus on a subgroup of cardiomyopathy genes [TTN, FHL1, CSRP3, FLNC and PLN, coding for Titin, Four and a Half LIM domain 1, Muscle LIM Protein, Filamin C and Phospholamban, respectively], which, despite their diverse biological functions, all have important signalling functions in the heart, suggesting that disturbances in signalling networks can contribute to cardiomyopathies.
Indexed as
Identifiers
What OpenQuestion holds
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.