Adaptive Cellular Responsiveness to Electrical Stimulation at the Skin‐Electrode Interface
7 affiliations
- 1Department of Chemical and Biomolecular Engineering Korea Advanced Institute of Science and Technology (KAIST) Daejeon South Korea
- 2Center for Biomaterials Korea Institute of Science and Technology (KIST) Seoul South Korea
- 3KU‐KIST Graduate School of Converging Science and Technology Korea University Seoul South Korea
- 4Interdisciplinary Research Center for Biosystems and Machines King Fahd University of Petroleum & Minerals Dhahran Saudi Arabia
- 5Defense of Forensic Service, Criminal Investigation Command Ministry of National Defense Seoul South Korea
- 6Doping Control Center Korea Institute of Science and Technology (KIST) Seoul South Korea
- 7College of Medicine Ajou University Suwon South Korea
Abstract
Wearable electrical stimulation (ES) devices are emerging platforms for wound healing, where cellular responses at the skin‐electrode interface critically influence therapeutic outcomes. Here, we demonstrate that skin cells dynamically adapt to sustained ES by upregulating voltage‐gated calcium channels (VGCCs) and enhancing their sensitivity to electrical cues. Using a transparent indium tin oxide (ITO)‐based bioelectronic platform, we find that ES‐induced upregulation of the L‐type VGCC CaV1.3 amplifies intracellular calcium (Ca2+) influx during subsequent stimulation. ES delivered through a skin‐conformal ITO‐based wearable device similarly increases CaV1.3 expression in mouse wound tissue, accompanied by accelerated wound healing, enhanced collagen deposition, vascular remodeling, and changes in the CD206/iNOS macrophage‐associated marker balance. Pharmacological inhibition of L‐type VGCCs with nifedipine suppresses CaV1.3 upregulation and attenuates these regenerative responses, supporting a functional contribution of VGCC‐mediated Ca2+ signaling to ES‐assisted wound repair. Human skin cells further exhibit enhanced Ca2+ responsiveness and coordinated transcriptional and proteomic remodeling following sustained ES. These findings identify adaptive VGCC‐associated Ca2+ signaling as a key cellular mechanism underlying sustained ES responses at the bioelectronic interface.
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BibTeX
@article{chang2026adaptive,
title = {{Adaptive Cellular Responsiveness to Electrical Stimulation at the Skin‐Electrode Interface}},
author = {Yeon Jae Chang and Soon Jin Choi and Khandoker Asiqur Rahaman and Tae Kyoung Lee and Gwangbin Lee and Jaeyeon Jun and Hyeon‐Jeong Lee and Hophil Min and Hojeong Jeon and Jung Keun Hyun and Hyung‐Seop Han and Jimin Park},
journal = {Advanced Science},
year = {2026},
month = oct,
doi = {10.1002/advs.78525},
url = {https://doi.org/10.1002/advs.78525},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Adaptive Cellular Responsiveness to Electrical Stimulation at the Skin‐Electrode Interface
AU - Yeon Jae Chang
AU - Soon Jin Choi
AU - Khandoker Asiqur Rahaman
AU - Tae Kyoung Lee
AU - Gwangbin Lee
AU - Jaeyeon Jun
AU - Hyeon‐Jeong Lee
AU - Hophil Min
AU - Hojeong Jeon
AU - Jung Keun Hyun
AU - Hyung‐Seop Han
AU - Jimin Park
PY - 2026
DA - 2026/10/27
JO - Advanced Science
DO - 10.1002/advs.78525
UR - https://doi.org/10.1002/advs.78525
AB - Wearable electrical stimulation (ES) devices are emerging platforms for wound healing, where cellular responses at the skin‐electrode interface critically influence therapeutic outcomes. Here, we demonstrate that skin cells dynamically adapt to sustained ES by upregulating voltage‐gated calcium channels (VGCCs) and enhancing their sensitivity to electrical cues. Using a transparent indium tin oxide (ITO)‐based bioelectronic platform, we find that ES‐induced upregulation of the L‐type VGCC CaV1.3 amplifies intracellular calcium (Ca2+) influx during subsequent stimulation. ES delivered through a skin‐conformal ITO‐based wearable device similarly increases CaV1.3 expression in mouse wound tissue, accompanied by accelerated wound healing, enhanced collagen deposition, vascular remodeling, and changes in the CD206/iNOS macrophage‐associated marker balance. Pharmacological inhibition of L‐type VGCCs with nifedipine suppresses CaV1.3 upregulation and attenuates these regenerative responses, supporting a functional contribution of VGCC‐mediated Ca2+ signaling to ES‐assisted wound repair. Human skin cells further exhibit enhanced Ca2+ responsiveness and coordinated transcriptional and proteomic remodeling following sustained ES. These findings identify adaptive VGCC‐associated Ca2+ signaling as a key cellular mechanism underlying sustained ES responses at the bioelectronic interface.
SN - 2198-3844
ER -