ReviewPediatric discovery2024
Exploring contractile protein mechanisms and target medications for cardiomyopathic patients with diastolic dysfunction.
Review in Pediatric discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Hypertrophic cardiomyopathy: insights into pathophysiology and novel therapeutic strategies from clinical studies.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2025Review
- Exploring contractile protein mechanisms and target medications for cardiomyopathic patients with diastolic dysfunction.Pediatric discovery · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Genetic defects have been increasingly found in cardiomyopathies, which are often present with mutations in cardiac contractile proteins. These congenital defects involve numerous intracellular pathways and share several critical clinical features, such as systolic or diastolic dysfunction fostering the various cardiomyopathic phenotypes. Hypertrophic cardiomyopathy and restrictive cardiomyopathy (RCM) share a common pathological feature, that is, diastolic dysfunction. Studies have shown that mutations of contractile proteins, especially myosin heavy chain and troponin, are tightly associated with diastolic dysfunction in patients with Cardiomyopathies (CMs), including pediatric patients with CM. Therapeutics, including green tea extract (epigallocatechin gallate) and mavacamten, interact directly with these contractile proteins and have shown promising results. This article will review recent and contemporary research on diastolic dysfunction in CMs, especially hypertrophic cardiomyopathy and RCM, which include their target proteins, mechanisms, clinical diagnosis, and potential therapies.
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Registered trials
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