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Li Tu

Researcher at Xiamen University

Publications -  6
Citations -  105

Li Tu is an academic researcher from Xiamen University. The author has contributed to research in topics: Reactive oxygen species & TFEB. The author has an hindex of 5, co-authored 5 publications receiving 49 citations.

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Journal ArticleDOI

Tumor-Specific Endogenous FeII-Activated, MRI-Guided Self-Targeting Gadolinium-Coordinated Theranostic Nanoplatforms for Amplification of ROS and Enhanced Chemodynamic Chemotherapy.

TL;DR: ASA-MTX-GdⅢ NPs could be catalyzed by tumor-specific overexpressed endogenous FeⅡ ions to generate sufficient ROS for enhancing the main chemodynamic efficacy, which could exert a synergistic effect with the assistant chemotherapy of MTX.
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Self-recognizing and stimulus-responsive carrier-free metal-coordinated nanotheranostics for magnetic resonance/photoacoustic/fluorescence imaging-guided synergistic photo-chemotherapy

TL;DR: Self-recognizing and stimulus-responsive carrier-free metal-coordinated nanotheranostics that showed strongly synergistic potency for tumor photo-chemotherapy under the precise guidance of magnetic resonance/photoacoustic/fluorescence imaging, thereby achieving highly effective tumor curing efficiency.
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CuS/Prussian blue core-shell nanohybrid as an electrochemical sensor for ascorbic acid detection.

TL;DR: An electrochemical sensor based on core-shell nanostructured copper sulfide@Prussian blue composites (CuS@PB) was investigated for ascorbic acid (AA) detection, demonstrating a great prospect for quantitative detection to AA of various fields.
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Molybdenum Disulfide Quantum Dots Attenuates Endothelial-to-Mesenchymal Transition by Activating TFEB-Mediated Lysosomal Biogenesis.

TL;DR: Using in vitro transforming growth factor (TGF)-β-induced EndMT model, it is demonstrated that the cardiovascular protective effect of MoS2 QDs against EndMT acted through triggering T FEB nucleus translocation and restoring an impairment of autophagic flux, whereas genetic suppression of TFEB impaired the protective action of Mo S2 QD against End MT.
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Regulation of Autophagy Orchestrates Pyroptotic Cell Death in Molybdenum Disulfide Quantum Dot-Induced Microglial Toxicity.

TL;DR: It is shown that exposure of microglia to MoS2 QDs triggered NLRP3 inflammasome activation as revealed by the cleavage of the inactive precursor of caspase-1 to its active form and the increased release of downstream pro-inflammatory cytokines, resulting inmicroglia cell death that occurred through casp enzyme-1-dependent pyroptosis.