Evidence map›Paper›PMID 34605861›Full record

ArticleThe Journal of general physiology2021

Synchrony of sarcomeric movement regulates left ventricular pump function in the in vivo beating mouse heart.

Fuyu Kobirumaki-Shimozawa, Togo Shimozawa, Kotaro Oyama, Shunsuke Baba, Jia Li, Tomohiro Nakanishi, Takako Terui, William E Louch, Shin'ichi Ishiwata, Norio Fukuda

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

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  7. Regulation of myocardial contraction as revealed by intracellular CaThe journal of physiological sciences : JPS · 2024
    Review
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  12. Titin force in muscle cells alters lattice order, thick and thin filament protein formation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    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

10 authors at 4 institutions in 2 countries.

Fuyu Kobirumaki-Shimozawa *Department of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan.ORCID 0000-0001-7054-1935
Togo Shimozawa *Technical Division, School of Science, The University of Tokyo, Tokyo, Japan.
Kotaro Oyama *Department of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan.
Shunsuke BabaDepartment of Pediatrics, The Jikei University School of Medicine, Tokyo, Japan.
Jia LiInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.
Tomohiro NakanishiDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan.ORCID 0000-0001-9694-5700
Takako TeruiDepartment of Anesthesiology, The Jikei University School of Medicine, Tokyo, Japan.
William E LouchInstitute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.ORCID 0000-0002-0511-6112
Shin'ichi IshiwataDepartment of Physics, Faculty of Science and Engineering, Waseda University, Tokyo, Japan.
Norio FukudaDepartment of Cell Physiology, The Jikei University School of Medicine, Tokyo, Japan.ORCID 0000-0001-8978-8938
Jikei University School of Medicine · JPOslo University Hospital · NOThe University of Tokyo · JPWaseda University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sarcomeric contraction in cardiomyocytes serves as the basis for the heart's pump functions. It has generally been considered that in cardiac muscle as well as in skeletal muscle, sarcomeres equally contribute to myofibrillar dynamics in myocytes at varying loads by producing similar levels of active and passive force. In the present study, we expressed α-actinin-AcGFP in Z-disks to analyze dynamic behaviors of sequentially connected individual sarcomeres along a myofibril in a left ventricular (LV) myocyte of the in vivo beating mouse heart. To quantify the magnitude of the contribution of individual sarcomeres to myofibrillar dynamics, we introduced the novel parameter "contribution index" (CI) to measure the synchrony in movements between a sarcomere and a myofibril (from -1 [complete asynchrony] to 1 [complete synchrony]). First, CI varied markedly between sarcomeres, with an average value of ∼0.3 during normal systole. Second, when the movements between adjacent sarcomeres were asynchronous (CI < 0), a sarcomere and the ones next to the adjacent sarcomeres and farther away moved in synchrony (CI > 0) along a myofibril. Third, when difference in LV pressure in diastole and systole (ΔLVP) was lowered to <10 mm Hg, diastolic sarcomere length increased. Under depressed conditions, the movements between adjacent sarcomeres were in marked asynchrony (CI, -0.3 to -0.4), and, as a result, average CI was linearly decreased in association with a decrease in ΔLVP. These findings suggest that in the left ventricle of the in vivo beating mouse heart, (1) sarcomeres heterogeneously contribute to myofibrillar dynamics due to an imbalance of active and passive force between neighboring sarcomeres, (2) the force imbalance is pronounced under depressed conditions coupled with a marked increase in passive force and the ensuing tug-of-war between sarcomeres, and (3) sarcomere synchrony via the distal intersarcomere interaction regulates the heart's pump function in coordination with myofibrillar contractility.

Indexed as

MyofibrilsSarcomeresAnimalsDiastoleMiceMuscle ContractionMyocytes, Cardiac

Identifiers

PMID34605861
PMCPMC8493835
OpenAlexW3204271361

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.