ReviewHeart failure reviews2024
Molecular mechanisms and emerging therapies in wild-type transthyretin amyloid cardiomyopathy.
Review in Heart failure reviews, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 28 citations in OpenAlex.
- Cardiomyocyte-Specific Smad7 Protects the Pressure-Overloaded Heart, Inhibiting the Transforming Growth Factor-β Receptor 1/Smad2/3 Cascade.Journal of the American Heart Association · 2026Article
- [Diagnosis of Amyloidosis in Hand and Plastic Surgery Patients: Optimal Tissue Selection and Examination Methods for Early Detection].Handchirurgie, Mikrochirurgie, plastische Chirurgie : Organ der Deutschsprachigen Arbeitsgemeinschaft fur Handchirurgie : Organ der Deutschsprachigen Arbeitsgemeinschaft fur Mikrochirurgie der Peripheren Nerven und Gefasse : Organ der V... · 2026Review
- Rationale, Objectives and Study Design of the Taiwan Registry of Hypertrophic Cardiomyopathy (THIC).Acta Cardiologica Sinica · 2026Article
- Regulatory mechanisms and interactions of mitophagy and ketone body metabolism in cardiac metabolism.Frontiers in cardiovascular medicine · 2026Review
- The Arrhythmic Burden of Cardiac Amyloidosis: A Comprehensive Review.Heart views : the official journal of the Gulf Heart Association · 2026Review
- Mitochondrial Dysfunction in Cardiomyopathy and Heart Failure: From Energetic Collapse to Therapeutic Opportunity.Biomolecules · 2025Review
- Transthyretin abnormalities in amyotrophic lateral sclerosis: High molecular weight species in cerebrospinal fluid and stromal deposits in choroid plexus.Journal of neuropathology and experimental neurology · 2025Article
- Review
- [Amyloid and orthopedic pathology : Early diagnosis may allow live-saving treatment of systemic amyloidosis].Zeitschrift fur Rheumatologie · 2025Article
- Effects of tafamidis on serial [European journal of nuclear medicine and molecular imaging · 2025Article
- Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.ESC heart failure · 2025Review
- Atrial cardiomyopathy in cardiac amyloidosis: clinical imaging and manifestations.NPJ cardiovascular health · 2025Article
- Exploring Cardiac Sympathetic Denervation in Transthyretin-Mediated Hereditary Amyloidosis (ATTRv): Insights fromDiagnostics (Basel, Switzerland) · 2025Article
- Vitreous amyloidosis caused by Lys55Asn mutation in TTR with peripheral neuropathy onset: a case report of FAP-related complications.International journal of ophthalmology · 2025Article
- From Molecular to Radionuclide and Pharmacological Aspects in Transthyretin Cardiac Amyloidosis.International journal of molecular sciences · 2024Review
- A Snapshot of the Most Recent Transthyretin Stabilizers.International journal of molecular sciences · 2024Review
- Oxidative Stress in Transthyretin-Mediated Amyloidosis: An Exploratory Study.Antioxidants (Basel, Switzerland) · 2024Article
- Review
- Wild-type transthyretin cardiac amyloidosis: a case of multisystemic involvement and review of literature.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Wild-type transthyretin amyloid cardiomyopathy (ATTRwt-CM) is an underrecognized cause of heart failure due to misfolded wild-type transthyretin (TTRwt) myocardial deposition. The development of wild-type TTR amyloid fibrils is a complex pathological process linked to the deterioration of homeostatic mechanisms owing to aging, plausibly implicating multiple molecular mechanisms. The components of amyloid transthyretin often include serum amyloid P, proteoglycans, and clusterin, which may play essential roles in the localization and elimination of amyloid fibrils. Oxidative stress, impaired mitochondrial function, and perturbation of intracellular calcium dynamics induced by TTR contribute to cardiac impairment. Recently, tafamidis has been the only drug approved by the U.S. Food and Drug Administration (FDA) for the treatment of ATTRwt-CM. In addition, small interfering RNAs and antisense oligonucleotides for ATTR-CM are promising therapeutic approaches and are currently in phase III clinical trials. Newly emerging therapies, such as antibodies targeting amyloid, inhibitors of seed formation, and CRISPR‒Cas9 technology, are currently in the early stages of research. The development of novel therapies is based on progress in comprehending the molecular events behind amyloid cardiomyopathy. There is still a need to further advance innovative treatments, providing patients with access to alternative and effective therapies, especially for patients diagnosed at a late stage.
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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.