.png){kind=icon}
.png){kind=icon}
Return
Nanomaterial-mediated regulation of ion channels and calcium-centered ionic homeostasis in cancer therapy
.png){kind=icon}
OA
AI
M
N
X
Z
R
Z
X
L
DOI：10.1186/s12951-026-04893-2.png)
.png){kind=icon}
Original request for help.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
Ion channels govern membrane excitability, ionic gradients and intracellular signaling in cancer cells, with broad consequences for tumor progression, cell death, therapeutic resistance and remodeling of the tumor microenvironment. Yet conventional pharmacological agonists and blockers, as well as genetic interventions, often lack the spatial and temporal precision required for selective cancer therapy. Nanomaterials offer a route to overcome these limitations by confining ion channel modulation to tumor tissues, cellular membranes or subcellular organelles, and by enabling externally triggered or tumor-responsive control of channel activation, inhibition, silencing or engineered ion-transport. This review summarizes recent advances in nanomaterial-mediated regulation of ion channels and ionic homeostasis in cancer therapy, with particular attention to calcium-centered channel regulation and calcium homeostasis disruption, while also covering emerging K⁺, Na⁺, Cl⁻ and engineered ion-transport strategies. Across these platforms, programmable ionic perturbations can drive calcium overload, mitochondrial dysfunction, chloride imbalance, membrane potential collapse, apoptosis, immune remodeling and reversal of therapeutic resistance. These studies position nanomaterials not merely as delivery vehicles, but as active regulators of ionic circuits in cancer. Future work should define ionic dose, tumor selectivity, response durability and long-term safety with greater precision to enable the transition of ion channel nanomedicine from proof-of-concept studies to reproducible therapeutic translation.
Keywords:
Ion channels
Cancer nanomedicine
Ionic homeostasis
Stimulus-responsive nanomaterials
Calcium overload
Journal
IF:
12.6
Papers:
5.0K
Citations:
2.8W
Organization
Cited Papers