Biology directJul 16, 2026

Reducing ATP6V1A increases skin cell aging caused by UVB light

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Jul 17, 2026

Abstract

Knockdown of ATP6V1A exacerbates UVB-induced cellular senescence and impairs lysosomal function.

Lysosomes play a crucial role in degrading and recycling cellular components, impacting overall cell health.
V-ATPase is identified as a regulator of lysosomal function in the context of photoaging.
Knockdown of ATP6V1A leads to worsened cellular senescence and damaged lysosomal acidification.
Overexpression of ATP6V1A can alleviate keratinocyte senescence and improve lysosomal function.
Inhibition of V-ATPase with BafA1 worsens cellular senescence and autophagy suppression, effects partially reversible by ATP6V1A overexpression.
Overall, ATP6V1A is linked to enhanced autophagy and reduced cellular aging effects from UVB exposure.

Simplified

Photoaging is a form of premature skin aging mainly induced by long-term exposure to ultraviolet exposure. Lysosomes are key organelles responsible for the degradation and recycling of intracellular components and are essential for maintaining metabolic and nutrient homeostasis. Although lysosomal dysfunction is closely associated with cellular aging, the role of V-ATPase in regulating lysosomal function during photoaging remains incompletely understood. By screening a V-ATPase-targeted siRNA library and validating the results using publicly available single-cell transcriptomic datasets, we identified ATP6V1A as a key regulator of UVB-induced cellular senescence. Furthermore, ATP6V1A knockdown exacerbated the UVB-induced cellular senescence and impaired lysosomal acidification and membrane integrity, whereas ATP6V1A overexpression effectively alleviated keratinocyte senescence, lysosomal dysfunction and autophagy inhibition. Moreover, treatment with the V-ATPase inhibitor BafA1 aggregated cellular senescence phenotype and autophagy inhibition and this phenomenon partially reversed by ATP6V1A overexpression. Collectively, ATP6V1A promotes autophagy by regulating lysosomal function, thereby relieving UVB-induced cellular senescence.

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PubMed

Reducing ATP6V1A increases skin cell aging caused by UVB light

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