ArticleMolecular and cellular biochemistry2004
The slow skeletal muscle troponin T gene is expressed in developing and diseased human heart.
Article in Molecular and cellular biochemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Troponin: biology, molecular mechanisms, and multidimensional clinical applications.Molecular biomedicine · 2026Review
- A homozygous single-nucleotide variant inJournal of neuromuscular diseases · 2025Article
- Cardiovascular Biomarkers: Lessons of the Past and Prospects for the Future.International journal of molecular sciences · 2022Review
- Mechanisms of in utero cortisol effects on the newborn heart revealed by transcriptomic modeling.American journal of physiology. Regulatory, integrative and comparative physiology · 2019Article
- Differences in Contractile Function of Myofibrils within Human Embryonic Stem Cell-Derived Cardiomyocytes vs. Adult Ventricular Myofibrils Are Related to Distinct Sarcomeric Protein Isoforms.Frontiers in physiology · 2017Article
- Cardiac myosin binding protein-C plays no regulatory role in skeletal muscle structure and function.PloS one · 2013Article
- The functional properties of human slow skeletal troponin T isoforms in cardiac muscle regulation.The Journal of biological chemistry · 2012Article
- Toad heart utilizes exclusively slow skeletal muscle troponin T: an evolutionary adaptation with potential functional benefits.The Journal of biological chemistry · 2012Article
- Comparative transcriptional and biochemical studies in muscle of myotonic dystrophies (DM1 and DM2).Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2009Article
- Transient expression of fast troponin C transcripts in embryonic quail heart.Journal of muscle research and cell motility · 2005Article
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Authors and funding
6 authors.
Funding
Abstract
Cardiac muscle development is characterised by the activation of contractile protein genes and subsequent modulation of expression resulting, ultimately, in the formation of a mature four-chambered organ. Myocardial gene expression is also altered in the adult in response to pathological stimuli and this is thought to contribute to the altered contractile characteristics of the diseased heart. We have examined the expression of the slow skeletal troponin T (TnT) gene in the human heart during development and in disease using whole mount in situ hybridisation and real-time quantitative (TaqMan) polymerase chain reaction (PCR). Slow skeletal TnT mRNA shows transitory and regional expression in the early foetal heart, which occurs at different times in atria and ventricles. In ventricular myocardium, expression is seen in the outer epicardial layer at a time when the coronary circulation is being established. Expression was detected at low levels in the adult human heart and was significantly increased in end-stage heart failure. Similarly, expression was readily detectable during early rat heart development and was up-regulated in pressure overload hypertrophy in adult. Together these data show for the first time that slow skeletal TnT mRNA is readily detectable during early human heart development. They further suggest that slow skeletal TnT may be responsive to myocardial stress and that elevated levels may contribute to myocardial dysfunction in adult disease. (Mol Cell Biochem 263: 91-97, 2004).
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Registered trials
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