Caveolin-1 in Skin Protection Against Radiation-Induced Skin Injuries - Pathophysiological Mechanisms and New Avenues for Prevention

Sep 30, 2026

Uploaded by Rhys

The identification of caveolin-1 (CAV1) as a universal pathophysiological factor and target for treating multiple cutaneous conditions, and for protecting cells from genotoxic stress, opens new strategies to prevent radiation-induced skin injuries (RISIs). After irradiation, CAV1 rises rapidly with a peak at 30–60 min, alongside internalization of epidermal growth factor receptors involved in homologous recombination and non-homologous end-joining repair. Stronger protection may require pre-irradiation CAV1 upregulation via thermo-mechanical stress that reinforces the actin cytoskeleton or via >10 MHz and multi-frequency ultrasound, without reducing cancer radiosensitivity.

LanguageEnglish

CategoryHealthcare

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Pages11

Reading Time28 min

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Introduction

Caveolin-1 as a Universal Pathophysiological Factor and Target in Pathological Cutaneous Conditions

Perspective Caveolin-1 in Skin Protection Against Radiation-Induced Skin Injuries: Pathophysiological Mechanisms and New Avenues for Prevention Ilja L. Kruglikov Academic Editor: Joohyun Nam Received: 8 December 2025 Revised: 26 December 2025 Accepted: 30 December 2025 Published: 30 December 2025 Copyright: © 2025 by the author. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license. Scientific Department, Wellcomet GmbH, 76646 Bruchsal, Germany; i.kruglikov@wellcomet.de Abstract The identification of caveolin-1 (CAV1) as a universal pathophysiological factor and target for treating various cutaneous conditions and the recognition of its role as a universal factor and target in the protection of cells from genotoxic stress have opened new avenues for protecting skin against radiation-induced skin injuries (RISIs) . A significant and rapid increase in CAV1 content in irradiated cells, reaching a maximum at 30–60 min after irradiation, coupled with internalization of epidermal growth factor receptors involved in the activation of homologous recombination and non-homologous end-joining repairing of double-strand breaks in affected cells, can protect the cells from irradiation to some degree. However, a higher level of protection can be achieved when the CAV1 content in the skin is increased before irradiation. Such an enhancement in the expression and translocation of CAV1 can be induced by the local application of thermo-mechanical stress with parameters inducing reinforcement of the actin cytoskeleton in treated cells. The application of very-high-frequency ultrasound waves with frequencies above 10 MHz or combined multi-frequency ultrasound waves can provide new means of protecting against RISIs during radiation therapy without reducing the radiosensitivity of cancer cells. Keywords: radiation-induced skin injuries; caveolin-1; prevention; therapy 1. Introduction Radiation-induced skin injuries (RISIs) are common complications of radiation therapy observed in 85–95% of treated patients, ranging from transient radiation dermatitis to chronic skin ulceration, radiation-induced keratosis, and fibrosis [1] . RISIs can lead to mildto-severe skin reactions; develop over several days or weeks after therapy or appear as late reactions months or even years after irradiation; induce pain; and result in long-lasting and significant reduction in quality of life. Early efforts to counteract RISI appearance were directed toward improving radiation schedules to reduce the effective dose of radiation, in order to remain under the threshold dose for corresponding side effects. Later, attention was switched to the mechanisms responsible for RISIs [2] to improve their treatment and provide some degree of skin protection. It is widely accepted that the most serious effects of ionizing radiation (IR) are related to the production of DNA damage in the form of double-strand breaks (DSBs) . DSBs can lead to either premature cell senescence or cell death, accompanied by severe tissue reactions such as ulceration and necrosis. Irradiated tissue exhibits chronic inflammation with significant secretion of proinflammatory factors [3] . This process is connected to the activation of the complement system in the skin, leading to the production of anaphylatoxins C3a and C5a [4], which are the chemo-attractants for inflammatory immune cells. Additionally, IR induces premature senescence in keratinocytes, which adopt a special secretory phenotype and stimulate an inflammatory response in affected tissue [5] . Radiation-induced fibrosis was found to be related to enhanced TGF-ß expression in the skin, the level of which strongly correlates with fibrosis scoring [3], while the appearance of non-healing radiation ulcers is thought to be caused by long-term radiation-induced damage to the vascular endothelium [6] . Th

FAQs

What role does caveolin-1 (CAV1) play in radiation-induced skin injuries?

CAV1 is presented as a universal pathophysiological factor and target involved in protecting cells from genotoxic stress, thereby influencing RISIs development.

Why does increasing CAV1 before irradiation improve protection?

The article notes that irradiated cells show a rapid CAV1 increase peaking at 30–60 min, but higher protection is achieved when skin CAV1 is elevated prior to irradiation.

How can CAV1 be enhanced to prevent RISIs during radiation therapy?

The document proposes local thermo-mechanical stress to induce CAV1 expression and translocation, and it also describes using very-high-frequency (>10 MHz) or combined multi-frequency ultrasound to protect against RISIs without reducing cancer radiosensitivity.

Sep 30, 2026

Uploaded by Rhys