Evidence map›Paper›PMID 38041810›Full record

ArticleCell reports2023

The sinoatrial node extracellular matrix promotes pacemaker phenotype and protects automaticity in engineered heart tissues from cyclic strain.

Yao-Hui Sun, Hillary K J Kao, Phung N Thai, Regan Smithers, Che-Wei Chang, Dalyir Pretto, Sergey Yechikov, Sarah Oppenheimer, Amanda Bedolla, Brooke A Chalker and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Coordination of cardiogenesis in vivo and in vitro.Nature reviews. Molecular cell biology · 2026
    Review
  7. Review
  8. Tissue elasticity modulates cardiac pacemaker cell automaticity.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  9. Article
  10. Review
  11. Review
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

15 authors at 3 institutions in 1 country.

Yao-Hui SunDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA; Institute for Regenerative Cures and Stem Cell Program, University of California, Davis, Sacramento, CA 95817, USA.
Hillary K J KaoDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA; Institute for Regenerative Cures and Stem Cell Program, University of California, Davis, Sacramento, CA 95817, USA.
Phung N ThaiDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA.
Regan SmithersDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA; Institute for Regenerative Cures and Stem Cell Program, University of California, Davis, Sacramento, CA 95817, USA.
Che-Wei ChangDepartment of Pathology and Laboratory Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Dalyir PrettoDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA; Institute for Regenerative Cures and Stem Cell Program, University of California, Davis, Sacramento, CA 95817, USA.
Sergey YechikovDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA; Institute for Regenerative Cures and Stem Cell Program, University of California, Davis, Sacramento, CA 95817, USA.
Sarah OppenheimerDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA; Institute for Regenerative Cures and Stem Cell Program, University of California, Davis, Sacramento, CA 95817, USA; Bridges to Stem Cell Research Program, California State University, Sacramento, Sacramento, CA 95817, USA.
Amanda BedollaDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA; Institute for Regenerative Cures and Stem Cell Program, University of California, Davis, Sacramento, CA 95817, USA; Bridges to Stem Cell Research Program, California State University, Sacramento, Sacramento, CA 95817, USA.
Brooke A ChalkerDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA; Institute for Regenerative Cures and Stem Cell Program, University of California, Davis, Sacramento, CA 95817, USA; Bridges to Stem Cell Research Program, Cal Poly Humboldt, Humboldt, CA 95521, USA.
Rana GhobashyDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA; Institute for Regenerative Cures and Stem Cell Program, University of California, Davis, Sacramento, CA 95817, USA; Bridges to Stem Cell Research Program, California State University, Sacramento, Sacramento, CA 95817, USA.
Jan A NoltaInstitute for Regenerative Cures and Stem Cell Program, University of California, Davis, Sacramento, CA 95817, USA.
James W ChanDepartment of Pathology and Laboratory Medicine, University of California, Davis, Sacramento, CA 95817, USA.
Nipavan ChiamvimonvatDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA; Department of Veterans Affairs, Northern California Health Care System, Mather, CA 95655, USA.
Deborah K LieuDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of California, Davis, Davis, CA 95616, USA; Institute for Regenerative Cures and Stem Cell Program, University of California, Davis, Sacramento, CA 95817, USA. Electronic address: dklieu@ucdavis.edu.
California Institute for Regenerative Medicine · USUniversity of California, Davis · USVA Northern California Health Care System · US

Funding

Functional Interactions of Cardiac Ion ChannelsR01HL085844 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2007 to 2025
$7.3M
Training Program In Basic & Translational Cardiovascular ScienceT32HL086350 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Martin Cadeiras, David A. Liem · 2008 to 2026
$7.1M
Translational Study of Cardiac DysfunctionR01HL085727 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN, SIRISH, PADMINI · 2008 to 2022
$5.7M
Decoding the enigma of cardiac amplificationR01HL137228 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHIAMVIMONVAT, NIPAVAN · 2017 to 2020
$2.2M
Molecular Mechanisms of Atrial Fibrillation: A Multimodal AnalysisR01HL170520 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Nipavan Chiamvimonvat, Vladimir Filkov · 2024 to 2026
$1.8M
Forcing the sinoatrial node pacemaker functionR01HL159492 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Deborah K Lieu · 2023 to 2026
$1.6M
Cardiac Regenerative Therapy Using Gene-Edited Stem Cells to Improve Transplantation OutcomesR56HL167932 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI SIRISH, PADMINI · 2023 to 2023
$400k
Regulation of ion channels in the heartI01BX000576 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI CHIAMVIMONVAT, NIPAVAN · 2009 to 2019
–
Metabolomics study in patients post myocardial infarctionI01CX001490 · VA · VA NORTHERN CALIFORNIA HEALTH CARE SYS · PI CHIAMVIMONVAT, NIPAVAN · 2017 to 2021
–
BLRD VA I01 BX000576CSRD VA I01 CX001490NHLBI NIH HHS R01 HL085727NHLBI NIH HHS R01 HL085844NHLBI NIH HHS R01 HL137228NHLBI NIH HHS R01 HL159492NHLBI NIH HHS R01 HL170520NHLBI NIH HHS R56 HL167932NHLBI NIH HHS T32 HL086350
6 · The paper itself

Abstract

The composite material-like extracellular matrix (ECM) in the sinoatrial node (SAN) supports the native pacemaking cardiomyocytes (PCMs). To test the roles of SAN ECM in the PCM phenotype and function, we engineered reconstructed-SAN heart tissues (rSANHTs) by recellularizing porcine SAN ECMs with hiPSC-derived PCMs. The hiPSC-PCMs in rSANHTs self-organized into clusters resembling the native SAN and displayed higher expression of pacemaker-specific genes and a faster automaticity compared with PCMs in reconstructed-left ventricular heart tissues (rLVHTs). To test the protective nature of SAN ECMs under strain, rSANHTs and rLVHTs were transplanted onto the murine thoracic diaphragm to undergo constant cyclic strain. All strained-rSANHTs preserved automaticity, whereas 66% of strained-rLVHTs lost their automaticity. In contrast to the strained-rLVHTs, PCMs in strained-rSANHTs maintained high expression of key pacemaker genes (HCN4, TBX3, and TBX18). These findings highlight the promotive and protective roles of the composite SAN ECM and provide valuable insights for pacemaking tissue engineering.

Indexed as

Myocytes, CardiacSinoatrial NodeAnimalsHeart VentriclesMicePhenotypeSwinecalcium transientscardiomyocytesCP: Cell biologyCP: Developmental biologyextracellular matrixhuman induced pluripotent stem cellspacemakersinoatrial node

Identifiers

PMID38041810
PMCPMC10790625
OpenAlexW4389266337

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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.