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Molecular Mechanism and Treatment of Hemangioma

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 June 2025 | Viewed by 425

Special Issue Editor


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Guest Editor
Department of Pharmacology, School of Biomedical Sciences, UNSW Sydney, Sydney, NSW 2050, Australia
Interests: angiomas; cardiovascular diseases; endocrinology; microbiology; vascular biology

Special Issue Information

Dear Colleagues,

A hemangioma is a mostly benign vascular tumor originating from blood vessel cell types. Endothelial cell dysfunction, vessel wall orientation, and its perivascular environments are amongst the major contributing factors to the disease. A hemangioma can occur anywhere on the body, but mainly in skin and internal organs. Although most hemangioma does not require medical interventions, some hemangioma requires treatment depending on its location and severity. For example, cerebral cavernous hemangioma in the brain can rupture and bleed and cause seizures, stroke, or neurological deficits. Those that require treatment are limited to untargeted therapies such as beta blockers, corticosteroids, and surgery.

This Special Issue, entitled “Molecular Mechanism and Treatment of Hemangioma”, aims to define and improve our understanding of the molecular mechanisms of hemangioma pathogenesis in order to develop targeted therapies to prevent and treat hemangioma. This Special Issue invites (but is not limited to) studies that provide an overview of the role of inflammation, oxidative stress, epigenetics, mechnotransduction, microbiology, environmental factors, and molecular mechanisms in the pathogenesis of hemangioma. Studies on the molecular mechanisms associated with small-vessel diseases are also welcomed, including rare disorders. As such, this Special Issue welcomes submissions of original research and review articles related to any aspect of the molecular mechanisms and pathogenesis of hemangioma with regard to identification, novel targets, and biomarkers.

Dr. Jaesung P. Choi
Guest Editor

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Keywords

  • hemangioma
  • angioma
  • cavernoma
  • vascular diseases
  • benign tumor
  • small vessels

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Published Papers (1 paper)

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Research

13 pages, 1387 KiB  
Article
Elevated Serum Protein Induced by Vitamin K Absence or Antagonist II Levels in Patients with Hepatic Hemangiomas
by Shigeo Maruyama, Tomomitsu Matono and Masahiko Koda
Int. J. Mol. Sci. 2025, 26(8), 3681; https://doi.org/10.3390/ijms26083681 - 13 Apr 2025
Viewed by 47
Abstract
Little is known about the effect of hepatic hemangiomas on protein induced by vitamin K absence or antagonist II (PIVKA-II). The aim of this study was to clarify the correlation of PIVKA-II levels with hepatic hemangiomas. In 335 consecutive patients with hepatic hemangiomas, [...] Read more.
Little is known about the effect of hepatic hemangiomas on protein induced by vitamin K absence or antagonist II (PIVKA-II). The aim of this study was to clarify the correlation of PIVKA-II levels with hepatic hemangiomas. In 335 consecutive patients with hepatic hemangiomas, ultrasonography (US), laboratory tests for liver function, serum levels of PIVKA-II and α-fetoprotein (AFP), and coagulation factors (platelets, prothrombin time (PT), fibrinogen, thrombin–antithrombin III complex (TAT), D-dimer, and fibrin and fibrinogen degradation products (FDPs)) as indicators of coagulation disorders were examined. PIVKA-II levels were significantly higher in the hemangioma group than in the control group (p < 0.0001), and significantly higher in the large hemangioma group (p < 0.0001). PIVKA-II levels in the hemangioma increase group were higher with increases in tumor size and abnormal coagulation factors, and those in the hemangioma decrease group were lower with decreases in tumor size and abnormal coagulation factors. PIVKA-II levels were significantly correlated with tumor size (p < 0.0001) and all coagulation factors (p < 0.05) except prothrombin. Hepatic hemangiomas were associated with elevated serum PIVKA-II levels, showing significant correlations with tumor size and coagulation disorders. PIVKA-II elevation was attributed to the increased production of prothrombin precursors caused by accelerated coagulation–fibrinolysis within hemangiomas. Full article
(This article belongs to the Special Issue Molecular Mechanism and Treatment of Hemangioma)
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