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제목	Graphene Quantum Dots Counteract Peritoneal Fibrosis by Binding Calcium Ions and Preventing Oxidative Stress
저자	Kyu Hong Kim
출판정보	2025; 2025(1):
키워드	Graphene Quantum Dots, CaCl2, Peritoneal fibrosis, ROS
초록	Divalent cations, including Ca2+, play a crucial role in the inflammation and fibrosis of the peritoneal membrane (PM). Accumulating evidence suggests that carbon-based nanomaterials, such as graphene quantum dots (GQDs), exhibit high affinity for calcium ions due to their surface oxygen functional groups and modulate calcium channels. In this study, we investigated the beneficial effects of GQDs in CaCl2-induced oxidative stress in human peritoneal mesothelial cells (HPMCs) and chlorhexidine gluconate (CG)-induced peritoneal fibrosis in a mouse model. The interaction between GQDs and Ca2+ was evaluated by photoluminescence (PL) using a spectrofluorometer with 365 nm excitation and zeta potential using Zetasizer NanoZS. The therapeutic efficacy of GQDs was evaluated in HPMCs with CaCl2-induced oxidative stress and in a CG-induced peritoneal fibrosis mouse model (CG: 0.1% daily in 15% EtOH; GQDs 20 or 40 mg/kg, every other day) by assessing ROS production, with additional analysis of DEGs and histology in the CG model. Zeta potential analysis confirmed that the negatively charged surface of GQDs (-37.9±1.8 mV) facilitates their binding with Ca2+ and showed high selectivity for Ca2+ (-13.4 1.1 mV) over Na+ (-27.5 3.1 mV) and K+ (-23.8 1.2 mV). This Ca2+ binding leads to significant PL quenching of GQDs compared to Na+, K+, Mg2+, also corresponds to their color changes and aggregation behavior. Transcriptomic profiling of GQDs-treated mice identified six downregulated pathways (p-value < 0.05) linked to calcium transport, endothelial apoptosis, and immune cell migration. GQDs reduced fibronectin and collagen deposition, suppressed immune infiltration, and enhanced Sod-2 activity in peritoneal tissue. In vitro, GQDs promoted oxidative degradation, correlating with Sod-2 expression. Notably, GQDs alleviated calcium abnormalities by suppressing L-type calcium channel genes (Cav 1.3 subtype; Cancnb3, Cacna1d, Cacnb1), mitigating calcium-driven fibrosis and oxidative stress. GQDs inhibit peritoneal fibrosis by binding Ca2+, reducing oxidative stress, and modulating calcium-dependent fibrotic and apoptotic pathways.
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