ArticleScientific reports2024
A chronic pro-inflammatory environment contributes to the physiopathology of actinic lentigines.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Decoding Hyperpigmentation from Biological Mechanisms to Actives with Clinically Proven Topical Efficacy: A Narrative Review.Dermatology and therapy · 2026Review
- Disrupted epigenetic regulation in human senile lentigines revealed by characterizing gene expression and DNA methylation alterations.Clinical epigenetics · 2026Article
- IBA-1Research square · 2026Article
- Review
- Unlocking Longevity in Aesthetic Dermatology: Epigenetics, Aging, and Personalized Care.International journal of dermatology · 2025Review
- Lysine Carboxymethyl Cysteinate, as a Topical Glutathione Precursor, Protects Against Oxidative Stress and UVB Radiation-Induced Skin Damage.Antioxidants (Basel, Switzerland) · 2025Article
- A Triple-Precursor Blend as a Topical Solution to Protect the Skin Against Environmental Damage.Biology · 2025Article
- Macrophage Phenotypic Switch and Obesity-Associated Metabolic Risk: Mechanisms and Targets.Oxidative medicine and cellular longevity · 2025Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Actinic lentigines (AL) or age spots, are skin hyperpigmented lesions associated with age and chronic sun exposure. To better understand the physiopathology of AL, we have characterized the inflammation response in AL of European and Japanese volunteers. Gene expression profile showed that in both populations, 10% of the modulated genes in AL versus adjacent non lesional skin (NL), i.e. 31 genes, are associated with inflammation/immune process. A pro-inflammatory environment in AL is strongly suggested by the activation of the arachidonic acid cascade and the plasmin pathway leading to prostaglandin production, along with the decrease of anti-inflammatory cytokines and the identification of inflammatory upstream regulators. Furthermore, in line with the over-expression of genes associated with the recruitment and activation of immune cells, immunostaining on skin sections revealed a significant infiltration of CD68+ macrophages and CD4
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