Evidence map›Paper›PMID 33246162›Full record

ReviewJournal of sport and health science2021

IGF1-PI3K-induced physiological cardiac hypertrophy: Implications for new heart failure therapies, biomarkers, and predicting cardiotoxicity.

Sebastian Bass-Stringer, Celeste M K Tai, Julie R McMullen

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of sport and health science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 55 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Precision Cardiogenomics in Athletes.International journal of molecular sciences · 2026
    Review
  5. Exercise-induced cardiac hypertrophy: cellular and molecular mechanisms of cardiac adaptation following physical activity.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2026
    Review
  6. Review
  7. Understanding the distinct role of PI3K(p110Frontiers in cardiovascular medicine · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Quercetin improves heart failure by inhibiting cardiomyocyte apoptosisNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    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

3 authors at 3 institutions in 1 country.

Sebastian Bass-StringerBaker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia; Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora, VIC 3086, Australia.
Celeste M K TaiBaker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia.
Julie R McMullenBaker Heart and Diabetes Institute, Melbourne, VIC 3004, Australia; Department of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora, VIC 3086, Australia; Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC 3004, Australia; Department of Physiology and Department of Medicine Alfred Hospital, Monash University, Melbourne, VIC 3004, Australia. Electronic address: julie.mcmullen@baker.edu.au.
Baker Heart and Diabetes Institute · AULa Trobe University · AUMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure represents the end point of a variety of cardiovascular diseases. It is a growing health burden and a leading cause of death worldwide. To date, limited treatment options exist for the treatment of heart failure, but exercise has been well-established as one of the few safe and effective interventions, leading to improved outcomes in patients. However, a lack of patient adherence remains a significant barrier in the implementation of exercise-based therapy for the treatment of heart failure. The insulin-like growth factor 1 (IGF1)-phosphoinositide 3-kinase (PI3K) pathway has been recognized as perhaps the most critical pathway for mediating exercised-induced heart growth and protection. Here, we discuss how modulating activity of the IGF1-PI3K pathway may be a valuable approach for the development of therapies that mimic the protective effects of exercise on the heart. We outline some of the promising approaches being investigated that utilize PI3K-based therapy for the treatment of heart failure. We discuss the implications for cardiac pathology and cardiotoxicity that arise in a setting of reduced PI3K activity. Finally, we discuss the use of animal models of cardiac health and disease, and genetic mice with increased or decreased cardiac PI3K activity for the discovery of novel drug targets and biomarkers of cardiovascular disease.

Indexed as

Heart FailurePhosphatidylinositol 3-KinasesAnimalsBiomarkersCardiomegalyCardiotoxicityHumansInsulin-Like Growth Factor IMiceMice, TransgenicPhosphatidylinositol 3-KinaseSignal TransductionBiomarkersIGF1 protein, humanInsulin-Like Growth Factor IPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesCardiac protectionCardiotoxicityExerciseHeart failureIGF1PI3KTherapies

Identifiers

PMID33246162
PMCPMC8724616
OpenAlexW3109822620

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.