Evidence map›Paper›PMID 37236659›Full record

ArticleLife science alliance2023

Estimation of crossbridge-state during cardiomyocyte beating using second harmonic generation.

Hideaki Fujita, Junichi Kaneshiro, Maki Takeda, Kensuke Sasaki, Rikako Yamamoto, Daiki Umetsu, Erina Kuranaga, Shuichiro Higo, Takumi Kondo, Yoshihiro Asano and 3 more

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.9field-weighted citation impact, top 9% of its field
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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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

13 authors at 4 institutions in 1 country.

Hideaki FujitaDepartment of Stem Cell Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Junichi KaneshiroLaboratory for Comprehensive Bioimaging, RIKEN Center for Biosystems Dynamics Research, Kobe, Japan.
Maki TakedaDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Kensuke SasakiLaboratory for Comprehensive Bioimaging, RIKEN Center for Biosystems Dynamics Research, Kobe, Japan.
Rikako YamamotoDepartment of Stem Cell Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Daiki UmetsuLaboratory for Histogenetic Dynamics, Graduate School of Life Sciences, Tohoku University, Sendai, Japan.
Erina KuranagaLaboratory for Histogenetic Dynamics, Graduate School of Life Sciences, Tohoku University, Sendai, Japan.
Shuichiro HigoDepartment of Medical Therapeutics for Heart Failure, Osaka University Graduate School of Medicine, Osaka, Japan.ORCID https://orcid.org/0000-0002-7473-7983
Takumi KondoDepartment of Medical Therapeutics for Heart Failure, Osaka University Graduate School of Medicine, Osaka, Japan.
Yoshihiro AsanoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
Yasushi SakataDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
Shigeru MiyagawaDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Tomonobu M WatanabeDepartment of Stem Cell Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan tomowatanabe@riken.jp.ORCID https://orcid.org/0000-0002-2420-4230
The University of Osaka · JPHiroshima University · JPRIKEN Center for Biosystems Dynamics Research · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Estimation of dynamic change of crossbridge formation in living cardiomyocytes is expected to provide crucial information for elucidating cardiomyopathy mechanisms, efficacy of an intervention, and others. Here, we established an assay system to dynamically measure second harmonic generation (SHG) anisotropy derived from myosin filaments depended on their crossbridge status in pulsating cardiomyocytes. Experiments utilizing an inheritable mutation that induces excessive myosin-actin interactions revealed that the correlation between sarcomere length and SHG anisotropy represents crossbridge formation ratio during pulsation. Furthermore, the present method found that ultraviolet irradiation induced an increased population of attached crossbridges that lost the force-generating ability upon myocardial differentiation. Taking an advantage of infrared two-photon excitation in SHG microscopy, myocardial dysfunction could be intravitally evaluated in a

Indexed as

Myocytes, CardiacSecond Harmonic Generation MicroscopyActomyosinMyocardiumMyosinsActomyosinMyosins

Identifiers

PMID37236659
PMCPMC10215972
OpenAlexW4378516036

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.