ArticleInternational journal of molecular sciences2025
Effect of Tigecycline on the Homeostasis of Human Epidermal Melanocytes and Fibroblasts.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Article
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Authors and funding
6 authors.
Funding
Abstract
Tigecycline is an antibiotic belonging to the glycylcycline group of tetracyclines. Similar to other tetracycline derivatives, tigecycline is used in dermatology because of its bacteriostatic effect. Despite an overall favorable safety profile, tetracyclines are associated with a spectrum of cutaneous adverse effects, notably pigmentary disorders and phototoxic reactions. These dermatologic manifestations are presumed to result from tigecycline's affinity for melanin biopolymer and its subsequent accumulation within the pigment-containing tissues. This study aimed to assess the impact of tigecycline on human normal skin cell homeostasis varied by melanin content. The study was conducted on HEMn-LP melanocytes and human dermal fibroblasts. The aim was achieved by determining the cell number, cell cycle, mitochondrial potential, and redox homeostasis and determining in silico the possibility of binding tigecycline to melanin biopolymers. In this study, it was shown that the cells more sensitive to tigecycline were HEMn-LP melanocytes. The obtained results showed that tigecycline decreased cell number in a dose-dependent manner. In addition, tigecycline was shown to reduce mitochondrial potential, increase the level of oxidized thiols, and increase ROS content in melanocytes, contributing to oxidative stress. In silico studies have shown that the binding of tigecycline to melanin may play a role in the induction of the toxic effects of tigecycline on the skin.
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Registered trials
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