ArticleResearch square2026
Development of Human iPSC-based Microphysiogical Models of Transthyretin Amyloid Cardiomyopathy.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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17 authors.
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Abstract
Transthyretin (TTR) amyloid cardiomyopathy (ATTR-CM) is a restrictive cardiac disease caused by the deposition of TTR in the heart. TTR is synthesized by hepatocytes and circulates as a homotetramer carrying complex for thyroxine and retinol. Mutations in TTR destabilize the tetramer promoting its dissociation into monomers that can enter the heart and aggregate into amyloid fibrils driving cytotoxicity, fibrosis, impaired electrical conductivity, and progressive cardiac dysfunction. Mechanistic studies and therapeutic development have been limited by the lack of physiologically relevant human preclinical models. Here we describe the creation of two
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