Evidence map›Paper›PMID 35861968›Full record

ArticleCirculation. Genomic and precision medicine2022

Human-Induced Pluripotent Stem Cell-Derived Cardiomyocyte Model for

Takumi Kondo, Shuichiro Higo, Mikio Shiba, Yasuaki Kohama, Satoshi Kameda, Tomoka Tabata, Hiroyuki Inoue, Shota Okuno, Shou Ogawa, Satoki Nakamura and 11 more

Abstract read
In one paragraph

Article in Circulation. Genomic and precision medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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

21 authors.

Takumi KondoDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).ORCID 0000-0001-8475-6240
Shuichiro HigoDepartment of Medical Therapeutics for Heart Failure (S. Higo).ORCID 0000-0002-7473-7983
Mikio ShibaDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).ORCID 0000-0003-4418-7834
Yasuaki KohamaDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).ORCID 0000-0001-5361-8662
Satoshi KamedaDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).
Tomoka TabataDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).
Hiroyuki InoueDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).
Shota OkunoDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).ORCID 0000-0002-8071-0090
Shou OgawaDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).
Satoki NakamuraOsaka Police Hospital, Osaka (S.N.).
Maki TakedaDepartment of Cardiovascular Surgery (M.T., E.I., J.L., L.L., S.M., Y.S.).ORCID 0000-0002-6434-8992
Emiko ItoDepartment of Cardiovascular Surgery (M.T., E.I., J.L., L.L., S.M., Y.S.).
Junjun LiDepartment of Cardiovascular Surgery (M.T., E.I., J.L., L.L., S.M., Y.S.).ORCID 0000-0002-7473-4918
Li LiuDepartment of Cardiovascular Surgery (M.T., E.I., J.L., L.L., S.M., Y.S.).
Yuki KuramotoDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).ORCID 0000-0001-7368-3584
Jong-Kook LeeDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).ORCID 0000-0001-9053-7781
Seiji TakashimaDepartment of Medical Biochemistry (S.T.), Osaka University Graduate School of Medicine, Suita, Osaka.
Shigeru MiyagawaDepartment of Cardiovascular Surgery (M.T., E.I., J.L., L.L., S.M., Y.S.).ORCID 0000-0003-0015-6569
Yoshiki SawaDepartment of Cardiovascular Surgery (M.T., E.I., J.L., L.L., S.M., Y.S.).ORCID 0000-0001-6132-9684
Shungo HikosoDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).ORCID 0000-0003-2284-1970
Yasushi SakataDepartment of Cardiovascular Medicine (T.K., M.S., S.K., T.T., H.I., S. Okuno, S.Ogawa, Y.K., J.-K.L., S. Hikoso, Y.S.).ORCID 0000-0002-5618-4721

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Δ160E mutation in

methodsWe identified a heterozygous in-frame deletion mutation (c.478_480del, p.Δ160E) in

resultsHetero-Δ160E-iPSC-CMs exhibited prolonged calcium decay, relaxation impairment, and hypertrophy compared to wild type-iPSC-CMs. Notably, these phenotypes were further exacerbated in Homo-Δ160E-iPSC-CMs. Overexpression of R-GECO-fused Δ160E mutant troponin T prolonged decay time and time to peak of the myofilament-localized calcium transient in iPSC-CMs, indicating that sarcomeric calcium retention with Δ160E may affect intracellular calcium concentration. High-content imaging analysis detected remarkable nuclear translocation of NFATc1, especially in Homo-Δ160E-iPSC-CMs, indicating that the Δ160E mutation promotes hypertrophic signaling pathway in a dose-dependent manner. Increased phosphorylation of CaMKIIδ (calcium/calmodulin-dependent protein kinase IIδ) and phospholamban at Thr17 was observed in Homo- and Hetero-Δ160E-iPSC-CMs. Epigallocatechin-3-gallate, a calcium desensitizing compound, shortened prolonged calcium decay and relaxation duration in Δ160E-iPSC-CMs.

conclusionsIsogenic iPSC-CMs recapitulate the prolonged calcium decay, relaxation impairment, and subsequent calcium-regulated signaling pathways caused by the

Indexed as

CardiomyopathiesCardiomyopathy, HypertrophicInduced Pluripotent Stem CellsCalciumCalcium-Calmodulin-Dependent Protein KinasesHumansInducible T-Cell Co-Stimulator ProteinMyocytes, CardiacTroponin TCalciumCalcium-Calmodulin-Dependent Protein KinasesInducible T-Cell Co-Stimulator ProteinTNNT2 protein, humanTroponin Tcardiomyopathy, hypertrophicheart failuremutationphenotypeprognosistroponin

Identifiers

PMID35861968
PMCPMC9584061

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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.