ReviewHeart failure reviews2015
Titin mutations: the fall of Goliath.
Review in Heart failure reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 19 citations in OpenAlex.
- Analysis ofCirculation. Genomic and precision medicine · 2025Article
- A Case Study Identified a New Mutation in theInternational journal of general medicine · 2025Article
- Exploring TTN variants as genetic insights into cardiomyopathy pathogenesis and potential emerging clues to molecular mechanisms in cardiomyopathies.Scientific reports · 2024Review
- Digenic Variants in theFrontiers in neuroscience · 2021Article
- Homozygous missense variant in the TTN gene causing autosomal recessive limb-girdle muscular dystrophy type 10.BMC medical genetics · 2019Article
- The giant titin: how to evaluate its role in cardiomyopathies.Journal of muscle research and cell motility · 2019Review
- A missense variant in the titin gene in Doberman pinscher dogs with familial dilated cardiomyopathy and sudden cardiac death.Human genetics · 2019Article
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- Exploring digenic inheritance in arrhythmogenic cardiomyopathy.BMC medical genetics · 2017Article
- Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017Review
- Deregulated CaScience advances · 2017Article
- The Role of Genetic Testing in the Identification of Young Athletes with Inherited Primitive Cardiac Disorders at Risk of Exercise Sudden Death.Frontiers in cardiovascular medicine · 2016Review
- Bringing It All Together: Bedside to Bench and Back Again.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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Titin (TTN), the largest protein in the human body, forms powerful elastic filaments along the sarcomere of cardiomyocytes. This multifunctional protein is involved in numerous cellular processes, including sarcomeric assembly, stabilization and mechanosensing. Along physiological sarcomere lengths, TTN is also the most important determinant of the passive tension of cardiac muscle. However, as the giant Goliath was brought down by David's slingshot, so single-base-pair mutations in the gene encoding TTN (TTN) can ultimately impair to some degree a normal cardiac function. Since the first report on the involvement of TTN mutations in the development of hypertrophic cardiomyopathy, in 1999, dozens of other mutations have been described and associated with the onset of cardiac disease. In this review, we aim to explore some of the mechanisms underlying the functions of TTN, as well as the pathophysiological consequences arising from the expression of abnormal TTN isoforms resulting from mutations located along TTN.
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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.