ArticlePediatric research2014
Propranolol inhibits growth of hemangioma-initiating cells but does not induce apoptosis.
Article in Pediatric research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Fibroblast adipogenesis restricts hemangioma growth through a PPARγ/Hippo-YAP/TAZ axis that promotes endothelial apoptosis and cell cycle arrest.Cell death discovery · 2026Article
- Analysis of Necroptosis-Related Genes and Immune Cell Infiltration in Infantile Hemangioma.Endocrine, metabolic & immune disorders drug targets · 2026Article
- β-Adrenergic Blockers Increase cAMP and Stimulate Insulin Secretion Through a PKA/RYR2/TRPM5 Pathway in Pancreatic β-Cells In Vitro.Pharmacology research & perspectives · 2025Article
- Overview of the Head and Neck Hemangiomas: a 5-year Retrospective Study.Materia socio-medica · 2023Article
- Infantile hemangiomas βPediatric research · 2022Article
- Epithelial-mesenchymal transition: a hallmark in pancreatic cancer stem cell migration, metastasis formation, and drug resistance.Journal of cancer metastasis and treatment · 2020Article
- Effect of combined low-dose oral prednisone with beta-adrenergic receptor antagonists for refractory infantile hemangiomas: retrospective cohort study in 76 patients.Annals of translational medicine · 2019Article
- The beta adrenergic receptor antagonist propranolol alters mitogenic and apoptotic signaling in late stage breast cancer.Biomedical journal · 2019Article
- Propranolol induces hemangioma endothelial cell apoptosis via a p53‑BAX mediated pathway.Molecular medicine reports · 2018Article
- Propranolol Targets Hemangioma Stem Cells via cAMP and Mitogen-Activated Protein Kinase Regulation.Stem cells translational medicine · 2016Article
- Propranolol: Effectiveness and Failure in Infantile Cutaneous Hemangiomas.Drug safety - case reports · 2015Article
- Educational paper: therapy of infantile haemangioma--history and current state (part II).European journal of pediatrics · 2015Review
- Adhesion molecule-mediated hippo pathway modulates hemangioendothelioma cell behavior.Molecular and cellular biology · 2014Article
- Propranolol enhanced adipogenesis instead of induction of apoptosis of hemangiomas stem cells.International journal of clinical and experimental pathology · 2014Article
- Approach to Infantile Hemangiomas.Indian journal of dermatologyArticle
- Mechanisms of propranolol action in infantile hemangioma.Dermato-endocrinologyArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundInfantile hemangioma (IH) is the most common tumor of infancy. The first-line therapy for IH is propranolol, a nonselective β-adrenergic receptor antagonist. However, mechanisms for the therapeutic effect of propranolol and regrowth of IH following cessation of treatment in some cases are not clear. We have recently shown that IH arises from multipotent stem cells. Whether IH stem cells are responsive to propranolol and are selectively targeted is unknown, and this is the focus of this study.
methodsIH stem cells were exposed to propranolol and were assayed for cellular and molecular alterations. We used endothelial cells (ECs) as controls and bone marrow-derived mesenchymal progenitor cells (bm-MPCs) as normal stem/progenitor counterparts to determine selectivity.
resultsOur results show that propranolol significantly reduced IH stem cell growth but failed to induce caspase-3 activation. Normal bm-MPCs and mature ECs showed maintained or increased caspase-3 activation and significantly reduced cyclin-D1 levels. We further show that IH stem cells may escape apoptosis by inducing antiapoptotic pathways.
conclusionThis study reveals that propranolol does not induce apoptosis in IH stem cells, which is in contrast with the result for ECs. Escape from apoptosis in IH stem cells may involve induction of antiapoptotic pathways.
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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.