TTR Stabilisation
The more stable, the more able.*
// Deposition of amyloid fibrils
The underlying cause of ATTR-CM
Transthyretin (TTR) is a tetrameric protein highly conserved through vertebrate evolution and involved in various physiological functions, including:
- Transport of thyroid hormone and retinol (vitamin A)
- Providing neuroprotection
- Supporting cognitive performance and memory
However, when the stability of TTR is compromised, misfolded TTR monomers can aggregate and form amyloid fibrils, which deposit in various organs. When amyloid fibrils deposit in the heart walls, symptoms like shortness of breath, fatigue, and dizziness can occur. Eventually, these deposits can lead to transthyretin amyloid cardiomyopathy (ATTR-CM).
* Within the general population, higher serum TTR (mg/dL) levels and increased TTR stabilisation are linked to a reduced risk of heart failure (R2=0.84).
- Referencesexpand_less
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- 2Vieira M, Saraiva MJ. BioMol Concepts. 2014;5(1):45–54.
- 3Hood CJ, et al. Curr Heart Fail Rep. 2022;19(5):356–363.
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- 5Garcia-Pavia P, et al. Eur J Heart Fail. 2021;23(4):512–526.
- 6Jain A, Zahra F. Transthyretin Amyloid Cardiomyopathy (ATTR-CM). 2023 Apr 27. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan. PMID: 34662045.
- 7Greve AM, et al. JAMA Cardiol. 2021;6(3):258–266.