ReviewJournal of biomedicine & biotechnology2010
Cardiac troponin mutations and restrictive cardiomyopathy.
Review in Journal of biomedicine & biotechnology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Meta-analysis of cardiomyopathy-associated variants in troponin genes identifies loci and intragenic hot spots that are associated with worse clinical outcomes.Journal of molecular and cellular cardiology · 2020Pooled it
- Therapeutic base editing alleviates restrictive cardiomyopathy.Cell reports. Medicine · 2026Article
- Potential Contribution ofCardiology research and practice · 2026Article
- Cardiac Sarcoidosis and Troponin T-Related Cardiomyopathy.JACC. Case reports · 2025Article
- Genetic Animal Models of Cardiovascular Pathologies.Biomedicines · 2025Review
- An FDA-approved drug structurally and phenotypically corrects the K210del mutation in genetic cardiomyopathy models.The Journal of clinical investigation · 2025Article
- Troponin I - a comprehensive review of its function, structure, evolution, and role in muscle diseases.Animal cells and systems · 2025Review
- Review
- Non-Canonical Localization of Cardiac Troponins: Expanding Functions or Causing Pathologies?International journal of molecular sciences · 2024Review
- Assessing Cardiac Contractility From Single Molecules to Whole Hearts.JACC. Basic to translational science · 2024Review
- Tale of two hearts: a TNNT2 hypertrophic cardiomyopathy case report.Frontiers in cardiovascular medicine · 2023Article
- Hypertension as One of the Main Non-Myocardial Infarction-Related Causes of Increased Cardiospecific Troponins: From Mechanisms to Significance in Current Medical Practice.Journal of clinical medicine research · 2022Review
- Intranuclear cardiac troponin I plays a functional role in regulatingGenes & diseases · 2022Article
- Cardiac Troponins as Biomarkers of Cardiac Myocytes Damage in Case of Arterial Hypertension: From Pathological Mechanisms to Predictive Significance.Life (Basel, Switzerland) · 2022Review
- The Metabolic Pathway of Cardiac Troponins Release: Mechanisms and Diagnostic Role.Cardiology research · 2022Review
- Features of the Metabolisms of Cardiac Troponin Molecules-Part 1: The Main Stages of Metabolism, Release Stage.Current issues in molecular biology · 2022Review
- Cardiomyocyte Dysfunction in Inherited Cardiomyopathies.International journal of molecular sciences · 2021Review
- Cardiomyocyte nuclearity and ploidy: when is double trouble?Journal of muscle research and cell motility · 2020Article
- Insights From Computational Modeling Into the Contribution of Mechano-Calcium Feedback on the Cardiac End-Systolic Force-Length Relationship.Frontiers in physiology · 2020Article
- The evolutionarily conserved C-terminal peptide of troponin I is an independently configured regulatory structure to function as a myofilament CaJournal of molecular and cellular cardiology · 2019Article
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
Mutations in sarcomeric proteins have recently been established as heritable causes of Restrictive Cardiomyopathy (RCM). RCM is clinically characterized as a defect in cardiac diastolic function, such as, impaired ventricular relaxation, reduced diastolic volume and increased end-diastolic pressure. To date, mutations have been identified in the cardiac genes for desmin, alpha-actin, troponin I and troponin T. Functional studies in skinned muscle fibers reconstituted with troponin mutants have established phenotypes consistent with the clinical findings which include an increase in myofilament Ca(2+) sensitivity and basal force. Moreover, when RCM mutants are incorporated into reconstituted myofilaments, the ability to inhibit the ATPase activity is reduced. A majority of the mutations cluster in specific regions of cardiac troponin and appear to be mutational "hot spots". This paper highlights the functional and clinical characteristics of RCM linked mutations within the troponin complex.
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.