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A catalase nanocapsule inhibits VSMCs proliferation and migration through PTEN/NLRP3 pathway
Yudan Wang1,2, Yu Chen3, Wenjuan Quan1
1Key Laboratory for Quality Evaluation of Bulk Herbs of Hunan Province, Hunan University of Chinese Medicine, Changsha, Hunan, China.
Background:
Aberrant VSMC proliferation, migration, and phenotypic switching drive vascular remodeling. Oxidative stress is pivotal, but effective antioxidants are limited.
Methods:
A catalase-loaded nanocapsule (CAT-nc) was developed for sustained ROS scavenging in Ang II-induced VSMCs.
Results:
CAT-nc reduced ROS, inhibited proliferation/migration, restored contractile phenotype via PTEN reactivation and NLRP3 suppression; PTEN inhibition abolished these effects.
Discussion:
Confirming the ROS-PTEN-NLRP3 axis, CAT-nc attenuates oxidative stress-driven VSMC switching, offering a promising nanotherapy for vascular diseases.
Insights
A novel catalase-loaded nanocapsule (CAT-nc) effectively scavenges reactive oxygen species (ROS), inhibiting vascular smooth muscle cell (VSMC) switching and offering a new nanotherapy for vascular diseases.
Area of Science:
- Biomedical Engineering
- Nanomedicine
- Vascular Biology
Background:
- Vascular remodeling involves aberrant vascular smooth muscle cell (VSMC) proliferation, migration, and phenotypic switching.
- Oxidative stress is a key factor in vascular remodeling, yet effective antioxidant therapies remain limited.
Purpose of the Study:
- To develop and evaluate a catalase-loaded nanocapsule (CAT-nc) for sustained reactive oxygen species (ROS) scavenging in VSMCs.
- To investigate the therapeutic potential of CAT-nc in mitigating oxidative stress-driven VSMC dysfunction.
Main Methods:
- A catalase-loaded nanocapsule (CAT-nc) was synthesized and characterized.
- CAT-nc was applied to Angiotensin II (Ang II)-induced VSMCs to assess its effects on ROS levels, proliferation, migration, and phenotype.
- The role of the PTEN/NLRP3 axis in mediating CAT-nc effects was examined.
Main Results:
- CAT-nc significantly reduced intracellular ROS levels in VSMCs.
- CAT-nc inhibited VSMC proliferation and migration.
- CAT-nc treatment restored the contractile VSMC phenotype, which was associated with PTEN reactivation and NLRP3 inflammasome suppression.
- Inhibition of PTEN abolished the beneficial effects of CAT-nc.
Conclusions:
- The developed CAT-nc effectively attenuates oxidative stress in VSMCs by scavenging ROS.
- CAT-nc demonstrates therapeutic potential for vascular diseases by targeting the ROS-PTEN-NLRP3 axis to prevent VSMC switching.
- CAT-nc represents a promising nanotherapy for vascular remodeling and related diseases.
