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Targeting TNF-SDH axis in macrophages reverses abnormal succinate metabolism and M1 polarization to alleviate UVB-induced skin damage
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DOI：10.1016/j.jphotobiol.2026.113433.png)
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Abstract
En 中文
Ultraviolet B (UVB) radiation is a major environmental factor causing skin damage, yet the actual role of macrophages in UVB-induced inflammatory remains incompletely understood. This study aimed to investigate the function and metabolic regulation of macrophages in UVB-induced skin injury. Clinical specimens from sun-exposed and non-sun-exposed human skin, murine models of acute and chronic UVB-induced damage, ex vivo skin co-culture system, and in vitro keratinocyte-macrophage co-culture systems were employed in our study. We found that depletion of macrophages by clodronate liposome significantly alleviated UVB-induced mouse skin damage. Further analysis revealed that UVB radiation promoted M1 polarization and induced metabolic dysregulation of macrophages. Pharmacological inhibition of TNF signaling using R7050 suppressed M1 polarization and ameliorated skin damage, while also rescuing UVB-induced metabolic alterations in macrophages. Importantly, restoration of succinate dehydrogenase (SDH) in macrophages reversed M1 polarization. These results demonstrated that macrophages contributed to UVB-induced skin injury via metabolic alterations and M1 polarization, processes orchestrated by the TNF-SDH axis. Targeting this pathway may represent a promising therapeutic strategy for UVB-induced skin pathologies.
Keywords:
Ultraviolet B
Skin damage
Macrophage
Metabolism
Macrophage polarization
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