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Angiogenesis in Chronic Inflammatory Skin Disorders
Open accessAbstract
Angiogenesis, the growth of new blood vessels from preexisting vessels, is associated with inflammation in various pathological conditions. Well-known angiogenetic factors include vascular endothelial growth factor (VEGF), angiopoietins, platelet-derived growth factor, transforming growth factor-β, and basic fibroblast growth factor. Yes-associated protein 1 (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) have recently been added to an important angiogenic factor. Accumulating evidence indicates associations between angiogenesis and chronic inflammatory skin diseases. Angiogenesis is deeply involved in the pathogenesis of psoriasis. VEGF, angiopoietins, tumor necrosis factor-a, interleukin-8, and interleukin-17 are unregulated in psoriasis and induce angiogenesis. Angiogenesis may be involved in the pathogenesis of atopic dermatitis, and in particular, mast cells are a major source of VEGF expression. Angiogenesis is an essential process in rosacea, which is induced by LL-37 from a signal cascade by microorganisms, VEGF, and MMP-3 from mast cells. In addition, angiogenesis by increased VEGF has been reported in chronic urticaria and hidradenitis suppurativa. The finding that VEGF is expressed in inflammatory skin lesions indicates that inhibition of angiogenesis is a useful strategy for treatment of chronic, inflammatory skin disorders.
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“Increasing real-world evidence also supports the durable efficacy and favorable long-term disease control achieved with selective IL-23 inhibitors [27,28].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [28]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Throughout this process, continuous exchange between keratinocytes and immune cells maintains a loop in which IL-23 sustains pathogenic T cells, IL-17 and IL-22 perpetuate epidermal alterations, and TNF-α amplifies inflammation across multiple cell types.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [28]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“These reflect activation of the IL-23/Th17 axis.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [28]
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“In psoriasis, histopathological findings include acanthosis, parakeratosis, neutrophilic microabscesses, and prominent dermal vascular proliferation.”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [28]
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“In severe or refractory cases, systemic agents such as methotrexate, cyclosporine, and acitretin are used to broadly suppress immune activation and keratinocyte turnover, but their long-term use is limited by toxicity and lack of pathway specificity [28].”
From The Cutaneous Immune Microenvironment in Selected Inflammatory Skin Diseases: Linking Histopathology, Mechanisms, and Targeted Therapy (2026) · cites this paper as [28]
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“Lee and others reported that LL‐37 accelerates the progression of the disease by activating the inflammatory body and inducing the release of angiogenic mediators, promoting the inflammatory signal transmission and vascular remodeling of rosacea [36].”
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Metadata
- Authors
- Lee, H. J., Hong, Y. J., & Kim, M.
- Affiliations
- The Catholic University of Korea Yeouido St. Mary's Hospital (KR)
- Corresponding author
- Kim, Miri
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2021-11-07
- Volume
- 22
- Issue
- 21
- Pages
- 12035
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC8584589
- OpenAlex
- W3212070111
- Semantic Scholar
- 5155b9747bd452bee5fcdea00619444cce1f7eac
- Cited by
- 211
- References
- 123
- Citations by year
- 2026: 31 · 2025: 63 · 2024: 55 · 2023: 43 · 2022: 19
- FWCI
- 3.07
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Research Foundation of Korea (2018R1D1A1B07044100 and 2019R1F1A1059460)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Health Sciences › Medicine › Oncology › Lymphatic System and Diseases
- Keywords
- angiogenesis, chronic inflammatory skin disease, psoriasis, atopic dermatitis, rosacea, chronic urticaria, hidradenitis suppurativa, vascular endothelial growth factor, angiopoietins, mast cells, YAP/TAZ signaling, angiogenesis inhibition, IL-17, interleukin-8, TNF-α, LL-37, MMP-3
- MeSH terms
- Animals, Chronic Disease, Dermatitis, Dermatitis, Atopic, Humans, Neovascularization, Pathologic, Psoriasis, Rosacea, Vascular Endothelial Growth Factor A, Angiopoietins
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