ReviewCardiovascular research2013
'Ryanopathy': causes and manifestations of RyR2 dysfunction in heart failure.
Review in Cardiovascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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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
56 citing papers in PubMed, 66 citations in OpenAlex.
- Metabolic stress exacerbates CaExperimental physiology · 2026Article
- Restoration of mitochondrial CaJournal of molecular and cellular cardiology · 2026Article
- Dynamic-Structure Redesign of Calmodulin Reveals Mechanistic Constraints on Ryr2 Regulation.bioRxiv : the preprint server for biology · 2026Article
- Ablation of mitochondrial calcium uniporter alleviates cardiac dysfunction in type 1 diabetes.Cell calcium · 2026Article
- Calcium release deficiency syndrome: an emerging ryanodinopathy.Frontiers in molecular biosciences · 2026Review
- Validation of novel predictors for early detection of cancer therapeutics-related cardiac dysfunction.Future cardiology · 2025Article
- Genetic variation in RYR1 is associated with heart failure progression and mortality in a diverse patient population.Frontiers in cardiovascular medicine · 2025Article
- The role of A-kinase anchoring proteins in cardiovascular diseases and recent advances.Frontiers in cell and developmental biology · 2025Review
- Conditional ablation of MCU exacerbated cardiac pathology in a genetic arrhythmic model of CPVT.Journal of molecular and cellular cardiology plus · 2024Article
- A structure-based computational model of IPBiophysical journal · 2024Article
- Neuron-Targeted Exosome Therapy: A Novel Approach for Treating Cardiogenic Dementia via RyR2 Inhibition.Medical hypotheses · 2024Article
- Role of sonic hedgehog signaling pathway in the regulation of ion channels: focus on its association with cardio-cerebrovascular diseases.Journal of physiology and biochemistry · 2023Review
- Function of a mutant ryanodine receptor (T4709M) linked to congenital myopathy.Scientific reports · 2023Article
- Article
- SR-Mitochondria Crosstalk Shapes Ca Signalling to Impact Pathophenotype in Disease Models Marked by Dysregulated Intracellular Ca Release.Cardiovascular research · 2022Article
- Molecular studies in familial dilated cardiomyopathy - A pilot study.International journal of cardiology. Heart & vasculature · 2022Article
- Predicting Heart Cell Types by Using Transcriptome Profiles and a Machine Learning Method.Life (Basel, Switzerland) · 2022Article
- Arrhythmogenic Remodeling in the Failing Heart.Cells · 2021Review
- MicroRNAs and Calcium Signaling in Heart Disease.International journal of molecular sciences · 2021Review
- Mechanisms underlying pathological CaPflugers Archiv : European journal of physiology · 2021Review
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
The cardiac ryanodine receptor (RyR2), a Ca(2+) release channel on the membrane of the sarcoplasmic reticulum (SR), plays a key role in determining the strength of the heartbeat by supplying Ca(2+) required for contractile activation. Abnormal RyR2 function is recognized as an important part of the pathophysiology of heart failure (HF). While in the normal heart, the balance between the cytosolic and intra-SR Ca(2+) regulation of RyR2 function maintains the contraction-relaxation cycle, in HF, this behaviour is compromised by excessive post-translational modifications of the RyR2. Such modification of the Ca(2+) release channel impairs the ability of the RyR2 to properly deactivate leading to a spectrum of Ca(2+)-dependent pathologies that include cardiac systolic and diastolic dysfunction, arrhythmias, and structural remodelling. In this article, we present an overview of recent advances in our understanding of the underlying causes and pathological consequences of abnormal RyR2 function in the failing heart. We also discuss the implications of these findings for HF therapy.
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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.