ReviewBiochimica et biophysica acta2013
Calcium mishandling in diastolic dysfunction: mechanisms and potential therapies.
Review in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 47 citations in OpenAlex.
- Impact of Dimethyl Sulfoxide on Early Cardiotoxicity After Allogeneic Hematopoietic Stem Cell Transplantation.Cardiovascular toxicology · 2026Article
- Fatty Acids and Their Roles in Cardiac Physiology and Pathology: Mechanistic and Interventional Studies.Nutrients · 2026Review
- Sarcomeric remodelling in human heart failure unraveled by single molecule long read sequencing.EMBO molecular medicine · 2026Article
- Review
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- Machine learning-based classification of cardiac relaxation impairment using sarcomere length and intracellular calcium transients.Computers in biology and medicine · 2023Article
- Critical Requirements for the Initiation of a Cardiac Arrhythmia in Rat Ventricle: How Many Myocytes?Cells · 2022Article
- Lipotoxicity: a driver of heart failure with preserved ejection fraction?Clinical science (London, England : 1979) · 2021Review
- Cellular pathology of the human heart in Duchenne muscular dystrophy (DMD): lessons learned from in vitro modeling.Pflugers Archiv : European journal of physiology · 2021Review
- DMD Pluripotent Stem Cell Derived Cardiac Cells RecapitulateFrontiers in bioengineering and biotechnology · 2020Article
- Topoisomerase 2B Decrease Results in Diastolic DysfunctionFrontiers in cardiovascular medicine · 2020Article
- Characterization of biventricular alterations in myocardial (reverse) remodelling in aortic banding-induced chronic pressure overload.Scientific reports · 2019Article
- Decrease in membrane phospholipids unsaturation correlates with myocardial diastolic dysfunction.PloS one · 2018Article
- Proteomic analysis reveals an impaired CaScientific reports · 2017Article
- Cholesterol depletion impairs contractile machinery in neonatal rat cardiomyocytes.Scientific reports · 2017Article
- Effects of Modified Parvalbumin EF-Hand Motifs on Cardiac Myocyte Contractile Function.Biophysical journal · 2016Article
- Discovering miRNA Regulatory Networks in Holt-Oram Syndrome Using a Zebrafish Model.Frontiers in bioengineering and biotechnology · 2016Article
- Ageing-related cardiomyocyte functional decline is sex and angiotensin II dependent.Age (Dordrecht, Netherlands) · 2014Article
- Therapeutic interventions for heart failure with preserved ejection fraction: A summary of current evidence.World journal of cardiology · 2014Review
- Article
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 at 1 institution in 1 country.
Funding
Abstract
Diastolic dysfunction is characterized by slow or incomplete relaxation of the ventricles during diastole, and is an important contributor to heart failure pathophysiology. Clinical symptoms include fatigue, shortness of breath, and pulmonary and peripheral edema, all contributing to decreased quality of life and poor prognosis. There are currently no therapies available that directly target the heart pump defects in diastolic function. Calcium mishandling is a hallmark of heart disease and has been the subject of a large body of research. Efforts are ongoing in a number of gene therapy approaches to normalize the function of calcium handling proteins such as sarcoplasmic reticulum calcium ATPase. An alternative approach to address calcium mishandling in diastolic dysfunction is to introduce calcium buffers to facilitate relaxation of the heart. Parvalbumin is a calcium binding protein found in fast-twitch skeletal muscle and not normally expressed in the heart. Gene transfer of parvalbumin into normal and diseased cardiac myocytes increases relaxation rate but also markedly decreases contraction amplitude. Although parvalbumin binds calcium in a delayed manner, it is not delayed enough to preserve full contractility. Factors contributing to the temporal nature of calcium buffering by parvalbumin are discussed in relation to remediation of diastolic dysfunction. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Cardiac Pathways of Differentiation, Metabolism and Contraction.
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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.