ReviewCardiovascular research2019
Inhibition of GSK-3 to induce cardiomyocyte proliferation: a recipe for in situ cardiac regeneration.
Review in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
The trial behind it
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Who cites it
23 citing papers in PubMed.
- β-Eudesmol Alleviates Inflammatory Injury in Septic Cardiomyopathy Through Enhancing GSK3B Activity to Inhibiting IL-17-Mediated Chemokine Expression.Biochemical genetics · 2026Article
- A gene regulatory element modulates myosin expression and controls cardiomyocyte response to stress.Genome research · 2025Article
- MARCH5 Promotes Cardiac Hypertrophy by Regulating Akt/mTOR/Gsk-3β/GATA4 Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
- Review
- Beyond FOXO1: AS1842856 inhibits GSK3 to enhance cytotoxic effects in B-ALL.Blood advances · 2025Article
- Generation of mature epicardium derived from human-induced pluripotent stem cells via inhibition of mTOR signaling.Nature communications · 2025Article
- Cardiac repair using regenerating neonatal heart tissue-derived extracellular vesicles.Nature communications · 2025Article
- Statins and Pacing-Induced Atrial Myopathy: Unraveling Their Role in Atrioventricular Block Patients with Permanent Pacemakers.International journal of medical sciences · 2025Article
- Quantitative label-free digital holographic imaging of cardiomyocyte optical volume, nucleation, and cell division.Journal of molecular and cellular cardiology · 2024Article
- Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart-Part II: Molecular Mechanisms of Cardiac Regeneration.Journal of cardiovascular development and disease · 2023Review
- YAP/TAZ: Molecular pathway and disease therapy.MedComm · 2023Review
- Suxiao Jiuxin Pill alleviates myocardial ischemia-reperfusion injury through the ALKBH5/GSK3β/mTOR pathway.Chinese medicine · 2023Article
- Genome Editing and Cardiac Regeneration.Advances in experimental medicine and biology · 2023Article
- Yes-associated protein activation potentiates glycogen synthase kinase-3 inhibitor-induced proliferation of neonatal cardiomyocytes and iPS cell-derived cardiomyocytes.Journal of cellular physiology · 2022Article
- Conditional depletion of the acetyltransferase Tip60 protects against the damaging effects of myocardial infarction.Journal of molecular and cellular cardiology · 2022Article
- Crosstalk between GSK-3β-actuated molecular cascades and myocardial physiology.Heart failure reviews · 2021Review
- S-nitrosoglutathione reductase (GSNOR) deficiency accelerates cardiomyocyte differentiation of induced pluripotent stem cells.The journal of cardiovascular aging · 2021Article
- ALKBH5 regulates cardiomyocyte proliferation and heart regeneration by demethylating the mRNA of YTHDF1.Theranostics · 2021Article
- Cardiac Regeneration After Myocardial Infarction: an Approachable Goal.Current cardiology reports · 2020Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
With an estimated 38 million current patients, heart failure (HF) is a leading cause of morbidity and mortality worldwide. Although the aetiology differs, HF is largely a disease of cardiomyocyte (CM) death or dysfunction. Due to the famously limited amount of regenerative capacity of the myocardium, the only viable option for advanced HF patients is cardiac transplantation; however, donor's hearts are in very short supply. Thus, novel regenerative strategies are urgently needed to reconstitute the injured hearts. Emerging data from our lab and others have elucidated that CM-specific deletion of glycogen synthase kinase (GSK)-3 family of kinases induces CM proliferation, and the degree of proliferation is amplified in the setting of cardiac stress. If this proliferation is sufficiently robust, one could induce meaningful regeneration without the need for delivering exogenous cells to the injured myocardium (i.e. cardiac regeneration in situ). Herein, we will discuss the emerging role of the GSK-3s in CM proliferation and differentiation, including their potential implications in cardiac regeneration. The underlying molecular interactions and cross-talk among signalling pathways will be discussed. We will also review the specificity and limitations of the available small molecule inhibitors targeting GSK-3 and their potential applications to stimulate the endogenous cardiac regenerative responses to repair the injured heart.
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Registered trials
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.