ReviewJournal of clinical medicine2025
Transthyretin Amyloid Cardiomyopathy Treatment: An Updated Review.
Review in Journal of clinical medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Serum Transthyretin as a Prognostic and Therapeutic Biomarker in Transthyretin Amyloid Cardiomyopathy Patients Treated with Tafamidis.Journal of clinical medicine · 2026Article
- Review
- Hereditary transthyretin amyloid cardiomyopathy caused by the rare TTR p.Ser43Asn variant in an Asian family: a case report.Frontiers in cardiovascular medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transthyretin amyloid cardiomyopathy (ATTR-CM) is a progressive form of restrictive cardiomyopathy caused by the misfolding and deposition of transthyretin protein. What was once a condition that had little by way of treatment other than liver transplantation has now become a manageable disease due to revolutionary novel therapies. This review outlines therapeutic strategies aimed at halting or reversing disease progression. Current approaches include transthyretin (TTR) stabilizers such as tafamidis and acoramidis, as well as TTR silencers such as vutisiran. In addition, novel therapies under clinical investigation are emerging, such as gene-editing strategies and monoclonal antibodies targeting amyloid deposits. The aim of this paper is to investigate the current literature and ongoing clinical trials exploring treatment options for ATTR-CM. Transthyretin stabilizers and RNA silencers improve survival, functional capacity, and quality of life. Early-phase studies of gene-editing and monoclonal antibody therapies demonstrate promising amyloid-lowering effects. Stabilizers and silencers continue to constitute the standard therapy, while gene-editing and monoclonal antibodies offer potential as future treatments. The advent of a multitude of therapies for ATTR-CM holds promise for a future of targeted, personalized medicine for the treatment of this not-so-uncommon cause of heart failure.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.