Evidence map›Paper›PMID 31606277›Full record

ReviewSeminars in cell & developmental biology2020

Upstream regulation of the Hippo-Yap pathway in cardiomyocyte regeneration.

Michael A Flinn, Brian A Link, Caitlin C O'Meara

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Heart failure, inflammation and exercise.International journal of biological sciences · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Genome Editing and Cardiac Regeneration.Advances in experimental medicine and biology · 2023
    Article
  14. Review
  15. Review
  16. Measuring cardiomyocyte cell-cycle activity and proliferation in the age of heart regeneration.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  17. Review
  18. Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022
    Review
  19. mBioengineered · 2022
    Article
  20. Potential Therapeutic Applications of N-Cadherin Antagonists and Agonists.Frontiers in cell and developmental biology · 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

3 authors at 1 institution in 1 country.

Michael A FlinnDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI, USA.
Brian A LinkDepartment of Cell Biology, Neurobiology, and Anatomy, Medical College of Wisconsin, Milwaukee, WI, USA; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI, USA.
Caitlin C O'MearaDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA; Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI, USA; Genomics Sciences and Precision Medicine Center, Medical College of Wisconsin, Milwaukee, WI, USA. Electronic address: comeara@mcw.edu.
Medical College of Wisconsin · US

Funding

IL13 - A Novel Therapeutic Factor for Cardiac RegenerationR01HL141159 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI O'MEARA, CAITLIN C · 2019 to 2023
$2.1M
RPE Signaling in Ocular Health and DiseaseR01EY029267 · NEI · MEDICAL COLLEGE OF WISCONSIN · PI LINK, BRIAN A · 2018 to 2021
$1.8M
NEI NIH HHS R01 EY029267NHLBI NIH HHS R01 HL141159
6 · The paper itself

Abstract

The response of the adult mammalian heart to injury such as myocardial infarction has long been described as primarily fibrotic scarring and adverse remodeling with little to no regeneration of cardiomyocytes. Emerging studies have challenged this paradigm by demonstrating that, indeed, adult mammalian cardiomyocytes are capable of completing cytokinesis albeit at levels vastly insufficient to compensate for the loss of functional cardiomyocytes following ischemic injury. Thus, there is great interest in identifying mechanisms to guide adult cardiomyocyte cell cycle re-entry and facilitate endogenous heart regeneration. The Hippo signaling pathway is a core kinase cascade that functions to suppress the transcriptional co-activators Yap and Taz by phosphorylation and therefore cytoplasmic retention or phospho-degradation. This pathway has recently sparked interest in the field of cardiac regeneration as inhibition of Hippo kinase signaling or overdriving the transcriptional co-activator, Yap, significantly promotes proliferation of terminally differentiated adult mammalian cardiomyocytes and can restore function in failing mouse hearts. Thus, the Hippo pathway is an attractive therapeutic target for promoting cardiomyocyte renewal and cardiac regeneration. Although the core kinases and transcriptional activators of the Hippo pathway have been studied extensively over the last twenty years, the regulatory inputs of this pathway, particularly in vertebrates, are poorly understood. Recent studies have elucidated several upstream regulatory inputs to the Hippo pathway in adult mammalian cardiomyocytes that influence cell proliferation and heart regeneration. Considering upstream inputs to the Hippo pathway are thought to be context and cell type specific, targeting these various components could serve as a therapeutic approach for refining Hippo-Yap signaling in the heart. Here, we provide an overview of the emerging regulatory inputs to the Hippo pathway as they relate to mammalian cardiomyocytes and heart regeneration.

Indexed as

RegenerationSignal TransductionCell Cycle ProteinsHeartHippo Signaling PathwayHumansMyocytes, CardiacProtein Serine-Threonine KinasesTranscription FactorsCell Cycle ProteinsProtein Serine-Threonine KinasesTranscription FactorsYY1AP1 protein, humanCardiomyocyteHippo signalingRegeneration

Identifiers

PMID31606277
PMCPMC7263368
OpenAlexW2979711656

What OpenQuestion holds

Textmetadata
LicenceTDM
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.