In one paragraphArticle in The Journal of cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
16 authors.
Honghai LiuDepartment of Pediatrics, Weill Cornell Medical College, Cornell University, New York City, NY, USA.ORCID 0000-0002-0693-6083 Niyatie AmmanamanchiDepartment of Pediatrics, Weill Cornell Medical College, Cornell University, New York City, NY, USA.ORCID 0000-0002-9335-3512 Jocelyn D Mich-BassoDivision of Cardiology, and Institute for Pediatric Heart Regeneration and Therapeutics, Richard King Mellon Foundation Institute for Pediatric Research, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA.ORCID 0009-0003-1316-6851 Brian K PanamaPhysiology and Biophysics, The State University of New York, University at Buffalo , Buffalo, NY, USA.ORCID 0009-0004-9627-2576 Yao LiDivision of Cardiology, and Institute for Pediatric Heart Regeneration and Therapeutics, Richard King Mellon Foundation Institute for Pediatric Research, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA.ORCID 0000-0002-7872-1495 Winston HuangDepartment of Pediatrics, Weill Cornell Medical College, Cornell University, New York City, NY, USA.ORCID 0009-0009-6289-3928 Dena AlmeidaMicroscopy and Image Analysis Core, Weill Cornell Medical College, Cornell University , New York City, NY, USA.ORCID 0000-0002-7286-2027 Christopher M LewarchikDivision of Cardiology, and Institute for Pediatric Heart Regeneration and Therapeutics, Richard King Mellon Foundation Institute for Pediatric Research, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA.
Brendan LoDepartment of Pediatrics, Weill Cornell Medical College, Cornell University, New York City, NY, USA.ORCID 0009-0006-8766-1881 Michael GotthardtMax Delbrück Center for Molecular Medicine in the Helmholtz Association and German Center for Cardiovascular Research , Berlin, Germany.ORCID 0000-0003-1788-3172 Michael I KotlikoffDepartment of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA.ORCID 0000-0001-9879-1899 Wolfgang BaehrDepartment of Ophthalmology, Department of Neurobiology & Anatomy, Department of Biology, University of Utah Health Science Center, Salt Lake City, UT, USA.ORCID 0000-0001-5003-9550 Randall RasmussonPhysiology and Biophysics, The State University of New York, University at Buffalo , Buffalo, NY, USA.ORCID 0009-0005-6641-7209 Bernhard KühnDepartment of Pediatrics, Weill Cornell Medical College, Cornell University, New York City, NY, USA.ORCID 0000-0002-1855-7072 Funding
University of Utah, Core Vision Research GrantP30EY014800 · NEI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jun Yang · 2005 to 2026
$14.6MRETINAL PHOTORECEPTOR CYCLIC GMP PHOSPHODIESTERASER01EY008123 · NEI · UNIVERSITY OF UTAH · PI BAEHR, WOLFGANG · 1990 to 2019
$7.8MMechanistic clinical trial of β-blocker administration for reactivating cardiomyocyte division in Tetralogy of FallotR01HL155597 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI KUHN, BERNHARD · 2021 to 2025
$3.4MGenetic Resource for Optical SignalingR24HL120847 · NHLBI · CORNELL UNIVERSITY · PI KOTLIKOFF, MICHAEL I. · 2014 to 2018
$3.1MQuantification of the decline of heart muscle cell proliferation and its reversal in pediatric patientsR01HL151386 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI KUHN, BERNHARD · 2020 to 2023
$1.7MLamin B2 regulates nuclear remodeling in cardiomyocyte terminal differentiationR01HL151415 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI KUHN, BERNHARD · 2020 to 2023
$1.5MLeducq Foundation 15CVD03NEI NIH HHS P30 EY014800NEI NIH HHS R01 EY008123NEI NIH HHS R01EY08123NHLBI NIH HHS R01 HL151386NHLBI NIH HHS R01 HL151415NHLBI NIH HHS R01 HL155597NHLBI NIH HHS R24 HL120847NIH HHS R01HL151386NIH HHS R01HL151415NIH HHS R01HL155597NIH HHS R24HL120847Retina Research FoundationUniversity of UtahUPMC Children's Hospital of Pittsburgh
6 · The paper itselfAbstract
Heart muscle growth and regeneration require the proliferation of cardiomyocytes. Rapid pulsatile increases in cytosolic Ca2+ concentration, called calcium transients (CaTs), trigger cardiomyocyte contractions, but how cardiomyocytes adapt Ca2+ signaling during proliferation is largely unknown. Here, we show that cardiomyocyte proliferation requires changes in Ca2+ signaling. Cardiomyocytes undergo a sequence of CaT changes during M phase: CaT amplitudes begin to decline in prometaphase, reach a minimum in metaphase, rise during anaphase, and return to the original state in daughter cardiomyocytes. Spindle poles show decreased Ca2+ levels during prometaphase and metaphase. Localized reduction of Ca2+ levels at spindle poles is mediated by dynein 1-dependent SERCA2a accumulation. Active cyclin-dependent kinase 1 (CDK1) induces both the decrease in CaT amplitudes and the accumulation of SERCA2a at the spindle poles, whereas CDK1 inhibition reverses these effects. Forcing an increase in cytosolic Ca2+ levels by blocking SERCA2a during prometaphase and metaphase disrupts mitosis and produces binucleated cardiomyocytes, underscoring the essential role of Ca2+ signaling changes for cardiomyocyte proliferation.
Indexed as
CalciumCalcium SignalingCell DivisionCell ProliferationMyocytes, CardiacAnimalsCDC2 Protein KinaseCells, CulturedDyneinsMiceMitosisSarcoplasmic Reticulum Calcium-Transporting ATPasesSpindle ApparatusCalciumCDC2 Protein KinaseDyneinsSarcoplasmic Reticulum Calcium-Transporting ATPases
Identifiers
PMID42347846
PMCPMC13308196
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