Evidence map›Paper›PMID 37788558›Full record

ArticleStem cell research2023

Generation of two induced pluripotent stem cell lines from patients with cardiac amyloidosis carrying heterozygous transthyretin (TTR) mutation.

Bernardo Bonilauri, Hye Sook Shin, Min Htet, Christopher D Yan, Ronald M Witteles, Karim Sallam, Joseph C Wu

Abstract read
In one paragraph

Article in Stem cell research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Bernardo BonilauriStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Hye Sook ShinStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Min HtetStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Christopher D YanStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA; Greenstone Biosciences, Palo Alto, CA 94305, USA.
Ronald M WittelesStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Karim SallamStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Joseph C WuStanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Medicine, Division of Cardiology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: joewu@stanford.edu.

Funding

Project 3 (Mercola)P01HL141084 · NHLBI · STANFORD UNIVERSITY · PI Joseph C. Wu · 2019 to 2026
$21.1M
Single Cell Sequencing of Human iPSC-CM Subtype Identity and FunctionR01HL145676 · NHLBI · STANFORD UNIVERSITY · PI MARK MERCOLA, Joseph C. Wu · 2019 to 2026
$5.1M
Elucidating Anthracycline-Induced Cell Type-Specific Cardiovascular Toxicity with CRISPRi/a ScreensR01HL150693 · NHLBI · STANFORD UNIVERSITY · PI Ronglih Liao, Joseph C. Wu · 2021 to 2026
$4.1M
BIOREPOSITORY OF HUMAN INDUCED PLURIPOTENT STEM CELLSFORCARDIOVASCULAR DISEASES (BHIPSC-CVD) - TASK AREA B75N92020D00019 · NHLBI · STANFORD UNIVERSITY · PI WU, JOSEPH · 2021 to 2024
$4.0M
Elucidating ECM Signaling in Cardiac Organoids with Machine Learning and Single-cell MultiomicsR01HL163680 · NHLBI · STANFORD UNIVERSITY · PI RAJADAS, JAYAKUMAR, WONG, WING H. · 2022 to 2025
$2.5M
NHLBI NIH HHS 75N92020D00019NHLBI NIH HHS P01 HL141084NHLBI NIH HHS R01 HL145676NHLBI NIH HHS R01 HL150693NHLBI NIH HHS R01 HL163680
6 · The paper itself

Abstract

Specific mutations in the TTR gene are responsible for the development of variant (hereditary) ATTR amyloidosis. Here, we generated two human induced pluripotent stem cell (iPSC) lines from patients diagnosed with Transthyretin Cardiac Amyloidosis (ATTR-CM) carrying heterozygous mutation in the TTR gene (i.e., p.Val30Met). The patient-derived iPSC lines showed expression of high levels of pluripotency markers, trilineage differentiation capacity, and normal karyotype. The generation of these iPSC lines represents a great tool for modeling patient-specific amyloidosis in vitro, allowing the investigation of the pathological mechanisms related to the disease in different cell types and tissues.

Indexed as

Amyloid Neuropathies, FamilialInduced Pluripotent Stem CellsCell DifferentiationHumansMutationPrealbuminPrealbuminAmyloidCardiac amyloidosisiPSCPluripotencyStem cellsTransthyretinTTR

Identifiers

PMID37788558
PMCPMC10821799

What OpenQuestion holds

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Registered trials

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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.