ArticlePloS one2015
Executioner Caspase-3 and 7 Deficiency Reduces Myocyte Number in the Developing Mouse Heart.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 52 citations in OpenAlex.
- The paradigm-shifting roles of caspase-3 in cancer: from death towards resuscitation.Cancer cell international · 2026Review
- Comprehensive Transcriptomic and Proteomic Analysis of Severe Pressure Ulcer Patients Identifies Molecular Signatures Associated with Impaired T Cell Function.Biomolecules · 2025Article
- Caspase-3 deficiency inhibits the development and anti-tumor response of bone marrow-derived dendritic cells.Discover oncology · 2025Article
- Mammalian TatD DNase domain containing 1 (TATDN1) is a proteostasis-responsive gene with roles in ventricular structure and neuromuscular function.The FEBS journal · 2025Article
- Aerobic capacity and muscle proteome: Insights from a mouse model.Experimental physiology · 2025Article
- Absence of MCJ/DnaJC15 promotes brown adipose tissue thermogenesis.Nature communications · 2025Article
- The concealed side of caspases: beyond a killer of cells.Cellular and molecular life sciences : CMLS · 2024Review
- Exploring caspase functions in mouse models.Apoptosis : an international journal on programmed cell death · 2024Review
- Caspase-3 promotes oncogene-induced malignant transformation via EndoG-dependent Src-STAT3 phosphorylation.Cell death & disease · 2024Article
- The Urinary Glycopeptide Profile Differentiates Early Cardiorenal Risk in Subjects Not Meeting Criteria for Chronic Kidney Disease.International journal of molecular sciences · 2024Article
- Chrysin reduces heart endoplasmic reticulum stress-induced apoptosis by inhibiting PERK and Caspase 3-7 in high-fat diet-fed rats.Molecular biology reports · 2024Article
- Dependence of human cell survival and proliferation on the CASP3 prodomain.Cell death discovery · 2024Article
- p38γ/δ activation alters cardiac electrical activity and predisposes to ventricular arrhythmia.Nature cardiovascular research · 2023Article
- The roles of intracellular proteolysis in cardiac ischemia-reperfusion injury.Basic research in cardiology · 2023Review
- Review
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Disruption of Proteostasis by Natural Products and Synthetic Compounds That Induce Pervasive Unfolding of Proteins: Therapeutic Implications.Pharmaceuticals (Basel, Switzerland) · 2023Article
- 'Youthful' phenotype of c-KitCellular and molecular life sciences : CMLS · 2022Article
- Paradoxical roles of caspase-3 in regulating cell survival, proliferation, and tumorigenesis.The Journal of cell biology · 2022Review
- Protective Effects of Shenfuyixin Granule on HEvidence-based complementary and alternative medicine : eCAM · 2021Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Executioner caspase-3 and -7 are proteases promoting cell death but non-apoptotic roles are being discovered. The heart expresses caspases only during development, suggesting they contribute to the organ maturation process. Therefore, we aimed at identifying novel functions of caspases in heart development. We induced simultaneous deletion of executioner caspase-3 and -7 in the mouse myocardium and studied its effects. Caspase knockout hearts are hypoplastic at birth, reaching normal weight progressively through myocyte hypertrophy. To identify the molecular pathways involved in these effects, we used microarray-based transcriptomics and multiplexed quantitative proteomics to compare wild type and executioner caspase-deficient myocardium at different developmental stages. Transcriptomics showed reduced expression of genes promoting DNA replication and cell cycle progression in the neonatal caspase-deficient heart suggesting reduced myocyte proliferation, and expression of non-cardiac isoforms of structural proteins in the adult null myocardium. Proteomics showed reduced abundance of proteins involved in oxidative phosphorylation accompanied by increased abundance of glycolytic enzymes underscoring retarded metabolic maturation of the caspase-null myocardium. Correlation between mRNA expression and protein abundance of relevant genes was confirmed, but transcriptomics and proteomics indentified complementary molecular pathways influenced by caspases in the developing heart. Forced expression of wild type or proteolytically inactive caspases in cultured cardiomyocytes induced expression of genes promoting cell division. The results reveal that executioner caspases can modulate heart's cellularity and maturation during development, contributing novel information about caspase biology and heart development.
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