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Promoting Collateral Formation in Type 2 Diabetes Mellitus Using Ultra-small Nanodots with Autophagy Activation and ROS Scavenging

Overview
Publisher Biomed Central
Specialty Biotechnology
Date 2024 Mar 1
PMID 38429826
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Abstract

Background: Impaired collateral formation is a major factor contributing to poor prognosis in type 2 diabetes mellitus (T2DM) patients with atherosclerotic cardiovascular disease. However, the current pharmacological treatments for improving collateral formation remain unsatisfactory. The induction of endothelial autophagy and the elimination of reactive oxygen species (ROS) represent potential therapeutic targets for enhancing endothelial angiogenesis and facilitating collateral formation. This study investigates the potential of molybdenum disulfide nanodots (MoS NDs) for enhancing collateral formation and improving prognosis.

Results: Our study shows that MoS NDs significantly enhance collateral formation in ischemic tissues of diabetic mice, improving effective blood resupply. Additionally, MoS NDs boost the proliferation, migration, and tube formation of endothelial cells under high glucose/hypoxia conditions in vitro. Mechanistically, the beneficial effects of MoS NDs on collateral formation not only depend on their known scavenging properties of ROS (HO, •O, and •OH) but also primarily involve a molecular pathway, cAMP/PKA-NR4A2, which promotes autophagy and contributes to mitigating damage in diabetic endothelial cells.

Conclusions: Overall, this study investigated the specific mechanism by which MoS NDs mediated autophagy activation and highlighted the synergy between autophagy activation and antioxidation, thus suggesting that an economic and biocompatible nano-agent with dual therapeutic functions is highly preferable for promoting collateral formation in a diabetic context, thus, highlighting their therapeutic potential.

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Advances in Theranostic Approaches and Emerging Biomarkers of Diabetes Mellitus.

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References
1.
Ke S, Lai Y, Li L, Tu L, Wang Y, Ren L . Molybdenum Disulfide Quantum Dots Attenuates Endothelial-to-Mesenchymal Transition by Activating TFEB-Mediated Lysosomal Biogenesis. ACS Biomater Sci Eng. 2021; 5(2):1057-1070. DOI: 10.1021/acsbiomaterials.8b01253. View

2.
Fan Z, Dong J, Mu Y, Liu X . Nesfatin-1 protects against diabetic cardiomyopathy in the streptozotocin-induced diabetic mouse model via the p38-MAPK pathway. Bioengineered. 2022; 13(6):14670-14681. PMC: 9342195. DOI: 10.1080/21655979.2022.2066748. View

3.
Rehman K, Akash M . Mechanism of Generation of Oxidative Stress and Pathophysiology of Type 2 Diabetes Mellitus: How Are They Interlinked?. J Cell Biochem. 2017; 118(11):3577-3585. DOI: 10.1002/jcb.26097. View

4.
Yuan R, Li Y, Yang B, Jin Z, Xu J, Shao Z . LOXL1 exerts oncogenesis and stimulates angiogenesis through the LOXL1-FBLN5/αvβ3 integrin/FAK-MAPK axis in ICC. Mol Ther Nucleic Acids. 2021; 23:797-810. PMC: 7868718. DOI: 10.1016/j.omtn.2021.01.001. View

5.
Liu H, Liu P, Shi X, Yin D, Zhao J . NR4A2 protects cardiomyocytes against myocardial infarction injury by promoting autophagy. Cell Death Discov. 2018; 4:27. PMC: 5841341. DOI: 10.1038/s41420-017-0011-8. View