ReviewCardiovascular research2022
Titin (TTN): from molecule to modifications, mechanics, and medical significance.
Review in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 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.
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Who cites it
98 citing papers in PubMed, 129 citations in OpenAlex.
- Functional analysis ofMolecular therapy. Nucleic acids · 2026Article
- Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction.Journal of molecular and cellular cardiology plus · 2026Review
- Diastolic contributors in cardiomyocytes of a cardiometabolic HFpEF-like mouse model.The Journal of general physiology · 2026Article
- Nx3 Is a Z-Disk Structural and Signaling Hub That Is Reduced in Heart Failure.Circulation research · 2026Article
- Integration of multiple perspectives to understand the left ventricular pressure-volume relationship.Communications medicine · 2026Review
- TTNCell reports · 2026Article
- Transcriptomic Analysis ofInternational journal of molecular sciences · 2026Article
- Transcriptomic Analysis ofbioRxiv : the preprint server for biology · 2026Article
- The titin N2A-MARP signalosome constrains muscle longitudinal hypertrophy in response to stretch.eLife · 2026Article
- Transcript-aware rare genetic variant association analyses of cardiopulmonary traits in participants from the All of Us Research Program.Nature communications · 2026Article
- Whole-exome sequencing identifies matrisomal gene associations in monogenic cerebral small vessel disease.Journal of neurology · 2026Article
- Overexpression of Circular RNA circTTN Promotes Ferroptosis in Sepsis-Induced Cardiomyopathy.Journal of cellular and molecular medicine · 2026Article
- The clinical pathophysiology of atrial fibrillation: outstanding questions from bedside to bench and back.Physiological reviews · 2026Review
- Effects of chemical myosin II cross-bridge inhibitors on eccentric force production in skinned muscle fibres.Experimental physiology · 2026Article
- SORBS2 regulates diastolic function through cytoskeletal networks and calcium handling.Communications biology · 2026Article
- Inflammation, metabolism, and aging in heart failure with preserved ejection fraction: Mechanisms and treatment perspectives.Journal of translational internal medicine · 2026Article
- RBM20 isoform regulation by independent transcription start sites adapts alternative splicing in development and disease.Nature communications · 2026Article
- Right Heart Diastology, Where Are We Now?Circulation research · 2026Review
- Titin's P-zone domains A164-167 are essential for thick filament structural arrangement.The Journal of general physiology · 2026Article
- A primer on the methods of skeletal and cardiac muscle mechanics using permeabilized preparations.The Journal of general physiology · 2026Review
38 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The giant sarcomere protein titin is a major determinant of cardiomyocyte stiffness and contributor to cardiac strain sensing. Titin-based forces are highly regulated in health and disease, which aids in the regulation of myocardial function, including cardiac filling and output. Due to the enormous size, complexity, and malleability of the titin molecule, titin properties are also vulnerable to dysregulation, as observed in various cardiac disorders. This review provides an overview of how cardiac titin properties can be changed at a molecular level, including the role isoform diversity and post-translational modifications (acetylation, oxidation, and phosphorylation) play in regulating myocardial stiffness and contractility. We then consider how this regulation becomes unbalanced in heart disease, with an emphasis on changes in titin stiffness and protein quality control. In this context, new insights into the key pathomechanisms of human cardiomyopathy due to a truncation in the titin gene (TTN) are discussed. Along the way, we touch on the potential for titin to be therapeutically targeted to treat acquired or inherited cardiac conditions, such as HFpEF or TTN-truncation cardiomyopathy.
Indexed as
Identifiers
What Socratic 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 Socratic graph.