Evidence map›Paper›PMID 31231540›Full record

ArticleCell discovery2019

Single-cell imaging and transcriptomic analyses of endogenous cardiomyocyte dedifferentiation and cycling.

Yiqiang Zhang, Nuria Gago-Lopez, Ning Li, Zhenhe Zhang, Naima Alver, Yonggang Liu, Amy M Martinson, Avin Mehri, William Robb MacLellan

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.7field-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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Journal of the American Heart Association · 2026
    Article
  3. Sertad4 Regulates Pathological Cardiac Remodeling.bioRxiv : the preprint server for biology · 2026
    Article
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  18. Review
  19. Tnni3k influences cardiomyocyte S-phase activity and proliferation.Journal of molecular and cellular cardiology · 2023
    Article
  20. 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

9 authors at 1 institution in 1 country.

Yiqiang Zhang1Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA USA.
Nuria Gago-Lopez1Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA USA.
Ning Li1Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA USA.
Zhenhe Zhang1Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA USA.
Naima Alver1Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA USA.
Yonggang Liu1Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA USA.
Amy M Martinson2Center for Cardiovascular Biology, University of Washington, Seattle, WA USA.
Avin Mehri1Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA USA.
William Robb MacLellan1Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA USA.
University of Washington · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
Genetic Dissection of Cardiac Growth: The Role of c-MycR01HL070748 · NHLBI · UNIVERSITY OF WASHINGTON · PI MACLELLAN, WILLIAM ROBB · 2004 to 2020
$5.0M
Epigenetic Mechanisms of Myocardial RegenerationR56HL131898 · NHLBI · UNIVERSITY OF WASHINGTON · PI ZHANG, YIQIANG · 2016 to 2016
$438k
NHLBI NIH HHS R01 HL070748NHLBI NIH HHS R56 HL131898NIDDK NIH HHS P30 DK017047
6 · The paper itself

Abstract

While it is recognized that there are low levels of new cardiomyocyte (CM) formation throughout life, the source of these new CM generates much debate. One hypothesis is that these new CMs arise from the proliferation of existing CMs potentially after dedifferentiation although direct evidence for this is lacking. Here we explore the mechanisms responsible for CM renewal in vivo using multi-reporter transgenic mouse models featuring efficient adult CM (ACM) genetic cell fate mapping and real-time cardiomyocyte lineage and dedifferentiation reporting. Our results demonstrate that non-myocytes (e.g., cardiac progenitor cells) contribute negligibly to new ACM formation at baseline or after cardiac injury. In contrast, we found a significant increase in dedifferentiated, cycling CMs in post-infarct hearts. ACM cell cycling was enhanced within the dedifferentiated CM population. Single-nucleus transcriptomic analysis demonstrated that CMs identified with dedifferentiation reporters had significant down-regulation in gene networks for cardiac hypertrophy, contractile, and electrical function, with shifts in metabolic pathways, but up-regulation in signaling pathways and gene sets for active cell cycle, proliferation, and cell survival. The results demonstrate that dedifferentiation may be an important prerequisite for CM proliferation and explain the limited but measurable cardiac myogenesis seen after myocardial infarction (MI).

Indexed as

Cell growthMechanisms of disease

Identifiers

PMID31231540
PMCPMC6547664
OpenAlexW2948505506

What OpenQuestion holds

Textmetadata
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.