Related Experiment Video
Updated: Jan 13, 2026
12:37
Pharmacologic Induction of Epidermal Melanin and Protection Against Sunburn in a Humanized Mouse Model
Published on: September 7, 2013
18.7K
CPT1B-Mediated Fatty Acid Oxidation Induces Pigmentation in Solar Lentigo
Yueun Choi1,2, Uijeong Nam1,2, Jihan Kim1,3
1Translational-Transdisciplinary Research Center, Clinical Research Institute, Kyung Hee University Hospital at Gangdong, College of Medicine, Kyung Hee University, Seoul, Korea.
Pigment Cell & Melanoma Research
|October 28, 2025
Summary
Cellular senescence alters lipid metabolism. This study identifies carnitine palmitoyltransferase 1B (CPT1B) as a key driver in solar lentigo pathogenesis, suggesting CPT1B as a therapeutic target for age-related pigmentation.
Area of Science:
- Dermatology
- Metabolic research
- Cellular biology
Background:
- Cellular senescence is linked to metabolic changes, particularly in lipid metabolism.
- Solar lentigo (SL), an age-related disorder, involves senescent cell accumulation but its metabolic role is understudied.
- Carnitine palmitoyltransferase (CPT) enzymes are crucial for fatty acid oxidation and implicated in senescence-related diseases.
Purpose of the Study:
- To investigate the molecular and metabolic alterations in solar lentigo (SL) skin.
- To identify potential molecular markers and therapeutic targets for SL.
- To explore the role of lipid metabolism in the pathogenesis of age-related pigmentation disorders.
Main Methods:
- Integrated transcriptomic profiling (mRNA sequencing, differential gene expression analysis).
- Pathway enrichment analysis and metabolic flux simulations.
- Protein-protein interaction analysis and multi-omics approach, including a zebrafish model.
Main Results:
- Transcriptomic alterations were observed in genes associated with mitochondrial energy metabolism.
- Metabolic flux simulations indicated upregulated fatty acid oxidation pathways involving carnitine.
- Carnitine palmitoyltransferase 1B (CPT1B) was identified as a potential SL marker and implicated in melanogenesis.
Conclusions:
- CPT1B-mediated alterations in lipid metabolism are central to SL pathogenesis.
- Targeting CPT1B and related lipid metabolism pathways offers a novel therapeutic strategy for SL and other age-related pigmentation disorders.
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