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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: closed (20 June 2025) | Viewed by 1568

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 (2 papers)

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Research

39 pages, 7427 KiB  
Article
Molecular Mediated Angiogenesis and Vasculogenesis Networks
by Claudiu N. Lungu, Ionel I. Mangalagiu, Aurelia Romila, Aurel Nechita, Mihai V. Putz and Mihaela C. Mehedinti
Int. J. Mol. Sci. 2025, 26(13), 6316; https://doi.org/10.3390/ijms26136316 - 30 Jun 2025
Viewed by 526
Abstract
By stimulating living tissues with proper molecules, the angiogenesis and vasculogenesis processes can be observed. Prostaglandin E1 (PGE1), which is a molecule that widens blood vessels and which is used for several medical purposes, such as treating critical limb ischemia, is a typical [...] Read more.
By stimulating living tissues with proper molecules, the angiogenesis and vasculogenesis processes can be observed. Prostaglandin E1 (PGE1), which is a molecule that widens blood vessels and which is used for several medical purposes, such as treating critical limb ischemia, is a typical leading molecule in angiogenesis studies. Nevertheless, its involvement in vasculogenesis and morphogenesis is a more specific subject in the field of developmental biology and therapeutic research. Vasculogenesis is the embryonic phenomenon in which endothelial progenitor cells generate new blood vessels. This phenomenon is distinct and divergent from angiogenesis, which entails the creation of novel blood vessels extending from pre-existing ones. Morphogenesis is the biological phenomenon responsible for the development of an organism or its components into a specific shape. Embryonic development and tissue regeneration are essential components. Current research is investigating the broader consequences of prostaglandins, such as PGE1, in the fields of developmental biology and regenerative medicine. Gaining knowledge about the impact of PGE1 on morphogenesis could provide valuable insights into congenital vascular abnormalities and innovative approaches for tissue repair and regeneration, especially in limb ischemia. In this study, a histologic and morphogenesis study was carried out on Artemia salina napi (first stage of development) by simulating the angiogenesis and morphogenesis processes using PGE1 as the top molecule with vasoactive properties and a series of benopyridyne (3-aminoquinolines, 5-amino quinolines, 8-aminoquinolines, 8-hydroxyquinolines and quinolines, respectively). A series of 30 Artemia salina napi were exposed to the compound listed before. Also, a lot of 30 unexposed Artemia salina napi was taken into account. In total, 210 Artemia salina napi were studied as a model for angionensis and morphogenesis. The study used wet experiments together with imaging reconstruction and graph-generating methodologies. The results show that PGE1 can initiate the shape of the vessel formation. Also, some quinoline series have a pro-mild morphogenetic and angiogenetic effect. Overall, PGE1 plays a significant role in mediating vasculogenesis and morphogenesis through its vasodilatory, anti-inflammatory, and pro-proliferative effects on endothelial cells. PGE1 is involved mainly in increasing the length of the vessel, while the number of vascular branching has an all-simulating general impact. However, the molecules with mild vasculogenic effects tend to develop more complex, limited vascular networks, having a more localized role in the angiogenetic process. Overall imaging and graph analysis showed significant and distinct properties of the vascular network-derived graph. Full article
(This article belongs to the Special Issue Molecular Mechanism and Treatment of Hemangioma)
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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 516
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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