Evidence map›Paper›PMID 33178704›Full record

ReviewFrontiers in cell and developmental biology2020

Cardiomyocyte Proliferation and Maturation: Two Sides of the Same Coin for Heart Regeneration.

Ming-Tao Zhao, Shiqiao Ye, Juan Su, Vidu Garg

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

58 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. The Role of BAG3 Protein Interactions in Cardiomyopathies.International journal of molecular sciences · 2024
    Article
  18. Article
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Ming-Tao ZhaoCenter for Cardiovascular Research, The Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH, United States.
Shiqiao YeCenter for Cardiovascular Research, The Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH, United States.
Juan SuCenter for Cardiovascular Research, The Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH, United States.
Vidu GargCenter for Cardiovascular Research, The Abigail Wexner Research Institute, Nationwide Children's Hospital, Columbus, OH, United States.
Nationwide Children's Hospital · USThe Ohio State University · US

Funding

The Role of Notch in Calcific Aortic Valve DiseaseR01HL132801 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GARG, VIDU, LILLY, BRENDA J · 2016 to 2019
$2.6M
Molecular Mechanisms of Aortic Valve FormationR01HL121797 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GARG, VIDU · 2015 to 2018
$1.6M
Epigenetic Mechanisms Underlying Maternal Diabetes Associated Cardiac MalformationsR01HL144009 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GARG, VIDU · 2019 to 2022
$1.5M
NHLBI NIH HHS R01 HL121797NHLBI NIH HHS R01 HL132801NHLBI NIH HHS R01 HL144009
6 · The paper itself

Abstract

In the past few decades, cardiac regeneration has been the central target for restoring the injured heart. In mammals, cardiomyocytes are terminally differentiated and rarely divide during adulthood. Embryonic and fetal cardiomyocytes undergo robust proliferation to form mature heart chambers in order to accommodate the increased workload of a systemic circulation. In contrast, postnatal cardiomyocytes stop dividing and initiate hypertrophic growth by increasing the size of the cardiomyocyte when exposed to increased workload. Extracellular and intracellular signaling pathways control embryonic cardiomyocyte proliferation and postnatal cardiac hypertrophy. Harnessing these pathways could be the future focus for stimulating endogenous cardiac regeneration in response to various pathological stressors. Meanwhile, patient-specific cardiomyocytes derived from autologous induced pluripotent stem cells (iPSCs) could become the major exogenous sources for replenishing the damaged myocardium. Human iPSC-derived cardiomyocytes (iPSC-CMs) are relatively immature and have the potential to increase the population of cells that advance to physiological hypertrophy in the presence of extracellular stimuli. In this review, we discuss how cardiac proliferation and maturation are regulated during embryonic development and postnatal growth, and explore how patient iPSC-CMs could serve as the future seed cells for cardiac cell replacement therapy.

Indexed as

cardiac regenerationcardiac stem cell therapycardiomyocyte hypertrophycardiomyocyte maturationcardiomyocyte proliferationinduced pluriopotent stem cells

Identifiers

PMID33178704
PMCPMC7593613
OpenAlexW3092696254

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.