Evidence map›Paper›PMID 34665129›Full record

ArticleeLife2021

Human Erbb2-induced Erk activity robustly stimulates cycling and functional remodeling of rat and human cardiomyocytes.

Nicholas Strash, Sophia DeLuca, Geovanni L Janer Carattini, Soon Chul Heo, Ryne Gorsuch, Nenad Bursac

Open access · goldAbstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Virulence factors released fromJournal of dental sciences · 2022
    Article
  13. MAPK/ERK Pathway as a Central Regulator in Vertebrate Organ Regeneration.International journal of molecular sciences · 2022
    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

6 authors at 1 institution in 1 country.

Nicholas StrashDepartment of Cell Biology, Duke University, Durham, United States.ORCID 0000-0003-1907-0925
Sophia DeLucaDepartment of Cell Biology, Duke University, Durham, United States.
Geovanni L Janer CarattiniDepartment of Biomedical Engineering, Duke University, Durham, United States.
Soon Chul HeoDepartment of Biomedical Engineering, Duke University, Durham, United States.
Ryne GorsuchDepartment of Biomedical Engineering, Duke University, Durham, United States.
Nenad BursacDepartment of Cell Biology, Duke University, Durham, United States.ORCID 0000-0002-5688-6061
Duke University · US

Funding

Training Program in Developmental & Stem Cell BiologyT32HD040372 · NICHD · DUKE UNIVERSITY · PI Terry H Lechler · 2001 to 2026
$8.9M
Integrated Cellular and Tissue Engineering for Ischemic Heart DiseaseU01HL134764 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BURSAC, NENAD, KAMP, TIMOTHY J. · 2016 to 2022
$7.7M
In Vitro and In Situ Engineering of Fibroblasts for Cardiac RepairR01HL132389 · NHLBI · DUKE UNIVERSITY · PI BURSAC, NENAD · 2016 to 2019
$2.0M
Investigating the Role of Polyploidy in the Maturation of hiPSC-derived CardiomyocytesF31HL156453 · NHLBI · DUKE UNIVERSITY · PI STRASH, NICHOLAS A · 2021 to 2023
$105k
NHLBI NIH HHS F31 HL156453NHLBI NIH HHS R01 HL132389NHLBI NIH HHS U01 HL134764NICHD NIH HHS T32 HD040372
6 · The paper itself

Abstract

Multiple mitogenic pathways capable of promoting mammalian cardiomyocyte (CM) proliferation have been identified as potential candidates for functional heart repair following myocardial infarction. However, it is unclear whether the effects of these mitogens are species-specific and how they directly compare in the same cardiac setting. Here, we examined how CM-specific lentiviral expression of various candidate mitogens affects human induced pluripotent stem cell-derived CMs (hiPSC-CMs) and neonatal rat ventricular myocytes (NRVMs) in vitro. In 2D-cultured CMs from both species, and in highly mature 3D-engineered cardiac tissues generated from NRVMs, a constitutively active mutant form of the human gene Erbb2 (cahErbb2) was the most potent tested mitogen. Persistent expression of cahErbb2 induced CM proliferation, sarcomere loss, and remodeling of tissue structure and function, which were attenuated by small molecule inhibitors of Erk signaling. These results suggest transient activation of Erbb2/Erk axis in CMs as a potential strategy for regenerative heart repair.

Indexed as

AnimalsCell ProliferationCells, CulturedErb-b2 Receptor Tyrosine KinasesExtracellular Signal-Regulated MAP KinasesGene Expression RegulationHumansInduced Pluripotent Stem CellsMyocytes, CardiacRatsRegenerationSignal TransductionERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesExtracellular Signal-Regulated MAP Kinasescardiomyocytecell biologyengineered cardiac tissueErbb2humaniPSCneonatal ratproliferationratregenerative medicinestem cells

Identifiers

PMID34665129
PMCPMC8589446
OpenAlexW3207147041

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.