ArticlePloS one2012
Epigallocatechin-3-gallate as a potential therapeutic drug for TTR-related amyloidosis: "in vivo" evidence from FAP mice models.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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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
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Pharmacological treatment for familial amyloid polyneuropathy.The Cochrane database of systematic reviews · 2020Pooled it
- Extracellular remodeling in patients with wild-type amyloidosis consuming epigallocatechin-3-gallate: preliminary results of T1 mapping by cardiac magnetic resonance imaging in a small single center study.Clinical research in cardiology : official journal of the German Cardiac Society · 2015Trial
- Green tea halts progression of cardiac transthyretin amyloidosis: an observational report.Clinical research in cardiology : official journal of the German Cardiac Society · 2012Trial
- [Terapias dirigidas en amiloidosis cardíaca por transtiretina: una revisión del contexto clínico contemporáneo].Archivos de cardiologia de Mexico · 2025Review
- Current Therapies and Future Horizons in Cardiac Amyloidosis Treatment.Current heart failure reports · 2024Review
- Molecular mechanisms and emerging therapies in wild-type transthyretin amyloid cardiomyopathy.Heart failure reviews · 2024Review
- Emerging Therapies for Transthyretin Amyloidosis.Current oncology reports · 2023Review
- A green tea extract catechin EGCg: Therapeutic potential for pediatric cardiomyopathies.Pediatric discovery · 2023Review
- 3D-Printed, Liquid-Filled Capsules of Concentrated and Stabilized Polyphenol Epigallocatechin Gallate, Developed in a Clinical Trial.Antioxidants (Basel, Switzerland) · 2023Article
- Status and Future Directions of Therapeutics and Prognosis of Cardiac Amyloidosis.Therapeutics and clinical risk management · 2023Review
- Hereditary transthyretin amyloidosis overview.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Review
- Cardiac Amyloidosis Treatment.Methodist DeBakey cardiovascular journal · 2022Review
- Searching for the Best Transthyretin Aggregation Protocol to Study Amyloid Fibril Disruption.International journal of molecular sciences · 2021Article
- Molecular Mechanisms of Cardiac Amyloidosis.International journal of molecular sciences · 2021Review
- A Brief Journey through Protein Misfolding in Transthyretin Amyloidosis (ATTR Amyloidosis).International journal of molecular sciences · 2021Review
- Chemical Chaperones Modulate the Formation of Metabolite Assemblies.International journal of molecular sciences · 2021Article
- Polyphenols Epigallocatechin Gallate and Resveratrol, and Polyphenol-Functionalized Nanoparticles Prevent Enterovirus Infection through Clustering and Stabilization of the Viruses.Pharmaceutics · 2021Article
- Activity of Selected Group of Monoterpenes in Alzheimer's Disease Symptoms in Experimental Model Studies-A Non-Systematic Review.International journal of molecular sciences · 2021Review
- Nutritional Value ofNutrients · 2021Article
- Green Tea Epigallocatechin-3-gallate (EGCG) Targeting Protein Misfolding in Drug Discovery for Neurodegenerative Diseases.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFamilial amyloidotic polyneuropathy (FAP) is a neurodegenerative disease caused by the extracellular deposition of mutant transthyretin (TTR), with special involvement of the peripheral nervous system (PNS). Currently, hepatic transplantation is considered the most efficient therapy to halt the progression of clinical symptoms in FAP since more than 95% of TTR is produced by the liver. However, less invasive and more reliable therapeutic approaches have been proposed for FAP therapy, namely based on drugs acting as inhibitors of amyloid formation or as amyloid disruptors. We have recently reported that epigallocatechin-3-gallate (EGCG), the most abundant catechin in green tea, is able to inhibit TTR aggregation and fibril formation, "in vitro" and in a cellular system, and is also able to disrupt pre-formed amyloid fibrils "in vitro". METHODOLOGY AND PRINCIPAL
findingsIn the present study, we assessed the effect of EGCG subchronic administration on TTR amyloidogenesis "in vivo", using well characterized animal models for FAP. Semiquantitative immunohistochemistry (SQ-IHC) and Western blot analysis of mice tissues after treatment demonstrated that EGCG inhibits TTR toxic aggregates deposition in about 50% along the gastrointestinal tract (GI) and peripheral nervous system (PNS). Moreover EGCG treatment considerably lowered levels of several biomarkers associated with non-fibrillar TTR deposition, namely endoplasmic reticulum (ER)-stress, protein oxidation and apoptosis markers. Treatment of old FAP mice with EGCG resulted not only in the decrease of non-fibrillar TTR deposition but also in disaggregation of amyloid deposits. Consistently, matrix metalloproteinase (MMP)-9 and serum amyloid P component (SAP), both markers of amyloid deposition, were also found reduced in treated old FAP mice. CONCLUSIONS AND SIGNIFICANCE: The dual effect of EGCG both as TTR aggregation inhibitor and amyloid fibril disruptor together with the high tolerability and low toxicity of EGCG in humans, point towards the potential use of this compound, or optimized derivatives, in the treatment of TTR-related amyloidoses.
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