Evidence map›Paper›PMID 39227655›Full record

ArticleScientific reports2024

Assessment of transthyretin instability in patients with wild-type transthyretin amyloid cardiomyopathy.

Takuya Iino, Manabu Nagao, Hidekazu Tanaka, Sachiko Yoshikawa, Junko Asakura, Makoto Nishimori, Masakazu Shinohara, Amane Harada, Shunsuke Watanabe, Tatsuro Ishida and 2 more

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Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
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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

12 authors.

Takuya IinoDivision of Cardiovascular Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Manabu NagaoDivision of Evidence-Based Laboratory Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-Cho, Chuo-Ku, Kobe, 650-0017, Japan. mnagao@med.kobe-u.ac.jp.
Hidekazu TanakaDivision of Cardiovascular Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Sachiko YoshikawaDivision of Cardiovascular Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Junko AsakuraDivision of Cardiovascular Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Makoto NishimoriDivision of Molecular Epidemiology, Kobe University Graduate School of Medicine, Kobe, Japan.
Masakazu ShinoharaDivision of Molecular Epidemiology, Kobe University Graduate School of Medicine, Kobe, Japan.
Amane HaradaCentral Research Laboratories, Sysmex Corporation, Kobe, Japan.
Shunsuke WatanabeBio-Diagnostic Reagent Technology Center, Sysmex Corporation, Kobe, Japan.
Tatsuro IshidaDivision of Cardiovascular Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Ken-Ichi HirataDivision of Cardiovascular Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Ryuji TohDivision of Evidence-Based Laboratory Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-Cho, Chuo-Ku, Kobe, 650-0017, Japan.

Funding

a Grant-in-Aid for Young Scientists (23K15102) from the Ministry of Education, Culture, Sports, Science and Technology of Japan 23K15102
6 · The paper itself

Abstract

The pathophysiology of variant transthyretin (TTR) amyloidosis (ATTRv) is associated with destabilizing mutations in the TTR tetramer. However, why TTR with a wild-type genetic sequence misfolds and aggregates in wild-type transthyretin amyloidosis (ATTRwt) is unknown. Here, we evaluate kinetic TTR stability with a newly developed ELISA system in combination with urea-induced protein denaturation. Compared with that in control patients, endogenous TTR in patients with wild-type transthyretin amyloid cardiomyopathy (ATTRwt-CM) exhibited thermodynamic instability, indicating that circulating TTR instability may be associated with the pathogenesis of ATTRwt as well as ATTRv. Our findings provide new insight into the underlying mechanisms of ATTRwt.

Indexed as

Amyloid Neuropathies, FamilialCardiomyopathiesPrealbuminAgedFemaleHumansKineticsMaleMiddle AgedMutationProtein StabilityPrealbuminTTR protein, humanAgingHeart failureHeart failure with preserved ejection fractionTransthyretinWild-type transthyretin amyloid cardiomyopathy

Identifiers

PMID39227655
PMCPMC11371834

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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.