ReviewPflugers Archiv : European journal of physiology2014
Maladaptive modifications in myofilament proteins and triggers in the progression to heart failure and sudden death.
Review in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 22 citations in OpenAlex.
- Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction.Journal of molecular and cellular cardiology plus · 2026Review
- Myofilament-associated proteins with intrinsic disorder (MAPIDs) and their resolution by computational modeling.Quarterly reviews of biophysics · 2023Review
- The Mechanism of Ajmaline and Thus Brugada Syndrome: Not Only the Sodium Channel!Frontiers in cardiovascular medicine · 2021Review
- Brugada Syndrome: Warning of a Systemic Condition?Frontiers in cardiovascular medicine · 2021Review
- Using 4-vinylcyclohexene diepoxide as a model of menopause for cardiovascular disease.American journal of physiology. Heart and circulatory physiology · 2020Article
- Brugada Syndrome: Oligogenic or Mendelian Disease?International journal of molecular sciences · 2020Review
- Epicardial ablation in genetic cardiomyopathies: a new frontier.European heart journal supplements : journal of the European Society of Cardiology · 2019Article
- Temperature-sensitive sarcomeric protein post-translational modifications revealed by top-down proteomics.Journal of molecular and cellular cardiology · 2018Article
- Calcium in Brugada Syndrome: Questions for Future Research.Frontiers in physiology · 2018Review
- Cardiac myofibrillar contractile properties during the progression from hypertension to decompensated heart failure.American journal of physiology. Heart and circulatory physiology · 2017Article
- Commentary: Next Generation Sequencing and Linkage Analysis for the Molecular Diagnosis of a Novel Overlapping Syndrome Characterized by Hypertrophic Cardiomyopathy and Typical Electrical Instability of Brugada Syndrome.Frontiers in physiology · 2017Article
- Liver Kinase B1 complex acts as a novel modifier of myofilament function and localizes to the Z-disk in cardiac myocytes.Archives of biochemistry and biophysics · 2016Article
- Sex dimorphisms of crossbridge cycling kinetics in transgenic hypertrophic cardiomyopathy mice.American journal of physiology. Heart and circulatory physiology · 2016Article
- Sarcomere length dependent effects on the interaction between cTnC and cTnI in skinned papillary muscle strips.Archives of biochemistry and biophysics · 2016Article
- Contribution of Post-translational Phosphorylation to Sarcomere-Linked Cardiomyopathy Phenotypes.Frontiers in physiology · 2016Article
- Dual Labeling Biotin Switch Assay to Reduce Bias Derived From Different Cysteine Subpopulations: A Method to Maximize S-Nitrosylation Detection.Circulation research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
In this review, we address the following question: Are modifications at the level of sarcomeric proteins in acquired heart failure early inducers of altered cardiac dynamics and signaling leading to remodeling and progression to decompensation? There is no doubt that most inherited cardiomyopathies are caused by mutations in proteins of the sarcomere. We think this linkage indicates that early changes at the level of the sarcomeres in acquired cardiac disorders may be significant in triggering the progression to failure. We consider evidence that there are rate-limiting mechanisms downstream of the trigger event of Ca(2+) binding to troponin C, which control cardiac dynamics. We discuss new perspectives on how modifications in these mechanisms may be of relevance to redox signaling in diastolic heart failure, to angiotensin II signaling via β-arrestin, and to remodeling related to altered structural rigidity of tropomyosin. We think that these new perspectives provide a rationale for future studies directed at a more thorough understanding of the question driving our review.
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.