ArticleThe Journal of clinical investigation2025
Regulation of TTN as a mechanism of and treatment for heart failure.
Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Cardiac resynchronization therapy and pulmonary artery banding in advanced heart failure infants with left ventricular dilated cardiomyopathy and left bundle branch block.Pediatric investigation · 2026Article
- Construction and validation of a palmitoylation-related prognostic model for lung adenocarcinoma based on integrated bioinformatics and machine learning.Translational cancer research · 2026Article
- HDAC5 Inhibition as a Therapeutic Strategy for Titin Deficiency-Induced Cardiac Remodeling: Insights from Human iPSC Models.Medicines (Basel, Switzerland) · 2025Article
- Integrated multi-sample transcriptomic analysis of COVID-19 patients against controls using a bioinformatics pipeline.Scientific reports · 2025Article
- Mapping the Somatic Mutation Landscape of Familial NF2-Related Schwannomatosis using Whole-Exome Sequencing.International journal of medical sciences · 2025Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Truncation variants in the gene TTN encoding titin are the most common cause of familial dilated cardiomyopathy (DCM), with both haploinsufficiency and "poison peptide" implicated as contributory mechanisms of disease. In this issue of the JCI, Kim et al. identify a highly conserved enhancer element approximately 500 bp downstream of the transcriptional start site of TTN in intron 1, which they demonstrated to be critical in regulating TTN expression. This work helps to further clarify the relative role of haploinsufficiency in TTN-related DCM and provides a potential target for therapies aimed at treating TTN-related DCM.
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Registered trials
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