ArticleCardiovascular research2023
Thymosin β4 and prothymosin α promote cardiac regeneration post-ischaemic injury in mice.
Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- An Integrated Cardiac Microtissue Proteome Map Extends Therapeutic Remodeling by Nanovesicles.Molecular & cellular proteomics : MCP · 2026Article
- The PIDDosome controls cardiomyocyte polyploidization during postnatal heart development.Cell death and differentiation · 2026Article
- Living myocardial slices as a model for testing cardiac pro-reparative gene therapies.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Generation of mature epicardium derived from human-induced pluripotent stem cells via inhibition of mTOR signaling.Nature communications · 2025Article
- The linker histone chaperone Prothymosin α (PTMA) is essential for efficient DNA damage repair and the recruitment of PARP1.Epigenetics & chromatin · 2025Article
- PTMA controls cardiomyocyte proliferation and cardiac repair by enhancing STAT3 acetylation.Science advances · 2025Article
- MiRNA Let-7i-5p-Contained Small Extracellular Vesicles from Macrophages Induce Nucleus Pulposus Cell Senescence via Targeting LIN28A.International journal of nanomedicine · 2025Article
- Expression levels of thymosin α1 in acute myocardial infarction patients and its correlation to cardiac function.Frontiers in cardiovascular medicine · 2025Article
- Hypoxia-responsive zinc finger E-box-binding homeobox 2 (ZEB2) regulates a network of calcium-handling genes in the injured heart.Cardiovascular research · 2024Article
- Cell cycle visualization tools to study cardiomyocyte proliferation in real-time.Open biology · 2024Review
- Transient induction of actin cytoskeletal remodeling associated with dedifferentiation, proliferation, and redifferentiation stimulates cardiac regeneration.Acta pharmaceutica Sinica. B · 2024Article
- Alternative polyadenylation and dynamic 3' UTR length is associated with polysome recruitment throughout the cardiomyogenic differentiation of hESCs.Frontiers in molecular biosciences · 2024Article
- Cardiomyocyte proliferation is suppressed by ARID1A-mediated YAP inhibition during cardiac maturation.Nature communications · 2023Article
- Regeneration of the heart: from molecular mechanisms to clinical therapeutics.Military Medical Research · 2023Review
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThe adult mammalian heart is a post-mitotic organ. Even in response to necrotic injuries, where regeneration would be essential to reinstate cardiac structure and function, only a minor percentage of cardiomyocytes undergo cytokinesis. The gene programme that promotes cell division within this population of cardiomyocytes is not fully understood. In this study, we aimed to determine the gene expression profile of proliferating adult cardiomyocytes in the mammalian heart after myocardial ischaemia, to identify factors to can promote cardiac regeneration. METHODS AND
resultsHere, we demonstrate increased 5-ethynyl-2'deoxyuridine incorporation in cardiomyocytes 3 days post-myocardial infarction in mice. By applying multi-colour lineage tracing, we show that this is paralleled by clonal expansion of cardiomyocytes in the borderzone of the infarcted tissue. Bioinformatic analysis of single-cell RNA sequencing data from cardiomyocytes at 3 days post ischaemic injury revealed a distinct transcriptional profile in cardiomyocytes expressing cell cycle markers. Combinatorial overexpression of the enriched genes within this population in neonatal rat cardiomyocytes and mice at postnatal day 12 (P12) unveiled key genes that promoted increased cardiomyocyte proliferation. Therapeutic delivery of these gene cocktails into the myocardial wall after ischaemic injury demonstrated that a combination of thymosin beta 4 (TMSB4) and prothymosin alpha (PTMA) provide a permissive environment for cardiomyocyte proliferation and thereby attenuated cardiac dysfunction.
conclusionThis study reveals the transcriptional profile of proliferating cardiomyocytes in the ischaemic heart and shows that overexpression of the two identified factors, TMSB4 and PTMA, can promote cardiac regeneration. This work indicates that in addition to activating cardiomyocyte proliferation, a supportive environment is a key for regeneration to occur.
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