Titin mutations in iPS cells define sarcomere insufficiency as a cause of dilated cardiomyopathy
Open accessAbstract
A giant disruption of the heart: Certain forms of heart failure originate from genetic mutations. Understanding how the culprit mutant proteins alter normal heart function could lead to more effective treatments. One candidate is the giant protein tintin, which is mutated in a subset of patients with dilated cardiomyopathy. Through a combination of patient-derived stem cells, tissue engineering, and gene editing, Hinson et al. found that disease-associated titin mutations disrupt the function of the contractile unit in heart muscle. As a result, the heart does not respond properly to mechanical and other forms of stress. Science , this issue p. 982
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The model identified 447 genes whose loss was predicted to shift cardiomyocytes towards the hypertrophic cardiomyopathy state, which were enriched for pathways including Titin binding and sarcomere organization known to impact hypertrophic cardiomyopathy pathogenesis.
“Overall, the model identified 447 genes whose loss was predicted to shift cardiomyocytes towards the hypertrophic cardiomyopathy state, which were enriched for pathways including Titin binding36 and sarcomere organization37 known to impact hypertrophic cardiomyopathy pathogenesis.”
From Transfer learning enables predictions in network biology (2023) · cites this paper as [36]
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Experimental — accuracy not yet measurediPSC-derived cardiomyocytes from DCM patients revealed that mutations including titin, troponin T, RBM20, and lamin are related to DCM through different molecular mechanisms.
“iPSC-derived cardiomyocytes from DCM patients revealed that several different mutations including titin [17], troponin T [18], RBM20 [19], and lamin [20,21,22] are related to DCM through different molecular mechanisms.”
From Utility of iPSC-Derived Cells for Disease Modeling, Drug Development, and Cell Therapy (2022) · cites this paper as [17]
Current state-of-the-art cardiac tissue models are well suited to measure contractile forces generated by cardiomyocytes, but modeling the cardiac pumping function using engineered cardiac tissues has been challenging.
“While current state-of-the-art cardiac tissue models are well suited to measure contractile forces generated by cardiomyocytes (11–13), modeling the cardiac pumping function using engineered cardiac tissues has been challenging.”
From Engineering a living cardiac pump on a chip using high-precision fabrication (2022) · cites this paper as [12]
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- Authors
- Hinson, J. T., Chopra, A., Nafissi, N., Polacheck, W. J., Benson, C. C., Swist, S., Gorham, J., Yang, L., Schafer, S., Sheng, C. C., Haghighi, A., Homsy, J., Hubner, N., Church, G., Cook, S. A., Linke, W. A., Chen, C. S., Seidman, J. G., & Seidman, C. E.
- Affiliations
- Brigham and Women's Hospital (US)
- Boston University (US)
- Harvard University (US)
- Beth Israel Deaconess Medical Center (US)
- Ruhr University Bochum (DE)
- Cardiovascular and Metabolic Sciences, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
- National Health Service (GB)
- Corresponding author
- Hinson, John T.
- Chopra, Anant
- Chen, Christopher S.
- Seidman, J. G.
- Seidman, Christine E.
- ORCID
- Venue
- Science
- Published
- 2015-08-28
- Volume
- 349
- Issue
- 6251
- Pages
- 982-986
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC4618316
- OpenAlex
- W2137802443
- Cited by
- 638
- References
- 37
- Citations by year
- 2026: 34 · 2025: 37 · 2024: 50 · 2023: 64 · 2022: 67 · 2021: 95 · 2020: 54 · 2019: 57 · 2018: 57 · 2017: 51 · 2016: 64 · 2015: 6 · 2014: 1
- FWCI
- 43.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion)
- National University of Singapore (submittedVersion)
- MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (submittedVersion)
- GoeScholar The Publication Server of the Georg-August-Universität Göttingen (Georg-August-Universität Göttingen) (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- Funders
- NIH (HG005550, EB017103, HL115553, HL007374, HL125807)
- Howard Hughes Medical Institute
- American Heart Association
- German Research Foundation (SFB 1002 TPB3)
- Leducq Foundation
- LaDue Fellowship
- Sarnoff Foundation
- NIHR Cardiovascular Biomedical Research Unit of Royal Brompton
- Harefield NHS Foundation Trust
- RESBIO Technology Resource for Polymeric Biomaterials
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Keywords
- titin, dilated cardiomyopathy, induced pluripotent stem cells, cardiac microtissues, missense mutations, cardiac contractility, cardiac remodeling, sarcomerogenesis
- MeSH terms
- Adrenergic beta-Agonists, Cardiomyopathy, Dilated, Cells, Cultured, Heart Rate, Humans, Isoproterenol, Myocardial Contraction, RNA, Sarcomeres, Stress, Physiological, Signal Transduction, Sequence Analysis, RNA, Mutation, Missense, Myocytes, Cardiac, Mutant Proteins, Induced Pluripotent Stem Cells, Connectin
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