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<p>Calcium ions (Ca²⁺) are ubiquitous signaling molecules that play important roles as messengers controlling a variety of cellular functions in eukaryotes. Intracellular Ca²⁺ is tightly regulated by a complex interplay between channels, pumps, and exchangers. Aging disrupts Ca²⁺ homeostasis, contributing to age-related diseases, such as neurodegenerative disorders. Previous studies have highlighted the role of Ca²⁺ in regulating actin cytoskeletal proteins in human dermal fibroblasts (HDFs). In this study, we investigated the effect of age on Ca²⁺ influx and efflux in HDFs to test the hypothesis that age-related perturbations in Ca²⁺ homeostasis are correlated with increased F-actin content in aged HDFs. We observed that aging leads to quantitative and functional changes in Ca²⁺ channels, resulting in differences in Ca²⁺ dynamics. Older HDFs showed reduced Ca²⁺ influx and accelerated outflow compared to neonatal and young cells, potentially inhibiting gelsolin activity and increasing F-actin content. Although Ca²⁺ alone cannot fully explain the age-dependent F-actin changes, our findings suggest that it plays an important role in cellular senescence.</p>

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Age-related changes in calcium ion influx and efflux capacity of human dermal fibroblasts

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月9日

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  • Se Jik Han,
  • Sangwoo Kwon,
  • Hae Jeong Park,
  • Kyung Sook Kim

摘要

Calcium ions (Ca²⁺) are ubiquitous signaling molecules that play important roles as messengers controlling a variety of cellular functions in eukaryotes. Intracellular Ca²⁺ is tightly regulated by a complex interplay between channels, pumps, and exchangers. Aging disrupts Ca²⁺ homeostasis, contributing to age-related diseases, such as neurodegenerative disorders. Previous studies have highlighted the role of Ca²⁺ in regulating actin cytoskeletal proteins in human dermal fibroblasts (HDFs). In this study, we investigated the effect of age on Ca²⁺ influx and efflux in HDFs to test the hypothesis that age-related perturbations in Ca²⁺ homeostasis are correlated with increased F-actin content in aged HDFs. We observed that aging leads to quantitative and functional changes in Ca²⁺ channels, resulting in differences in Ca²⁺ dynamics. Older HDFs showed reduced Ca²⁺ influx and accelerated outflow compared to neonatal and young cells, potentially inhibiting gelsolin activity and increasing F-actin content. Although Ca²⁺ alone cannot fully explain the age-dependent F-actin changes, our findings suggest that it plays an important role in cellular senescence.