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H₂S Click Delivery: Responsive Release for Multidimensional Therapy of Thoracic Aortic Dissection.

Yunpeng Luo¹, Daquan Wang², Gang Tan²

¹Clinical School of Thoracic, Department of Cardiovascular Surgery, Tianjin Medical University, Tianjin Chest Hospital, Tianjin, P. R. China.

Advanced Healthcare Materials

|December 4, 2025

Summary

A novel polymer, PSG12, delivers hydrogen sulfide (H2S) precisely to treat thoracic aortic dissection (TAD). This targeted therapy protects endothelial cells and improves survival rates in TAD mouse models, offering a promising new treatment for this cardiovascular emergency.

Keywords:

controlled drug release endothelial barrier protection gas click polymer hydrogen sulfide (H2S)thoracic aortic dissection (TAD)

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Area of Science:

Biomaterials Science
Cardiovascular Research
Drug Delivery Systems

Background:

Thoracic aortic dissection (TAD) is a life-threatening cardiovascular emergency with limited pharmacological treatments.
Endothelial dysfunction and reduced hydrogen sulfide (H2S) levels are key factors in TAD progression.
Current H2S therapies face challenges due to uncontrolled release and toxicity.

Purpose of the Study:

To develop a novel, controlled hydrogen sulfide (H2S)-releasing polymer for treating thoracic aortic dissection (TAD).
To evaluate the efficacy of the developed polymer (PSG12) in cellular and animal models of TAD.

Main Methods:

A glutathione (GSH)-responsive H2S-releasing polymer (PSG12) was synthesized using a gas-click polymerization strategy.
PSG12's H2S release kinetics and pharmacokinetic profile were characterized.
The therapeutic effects of PSG12 were assessed in TNF-α-challenged endothelial cells and BAPN-induced TAD mouse models.

Main Results:

PSG12 demonstrated tunable and sustained H2S release, maintaining therapeutic plasma levels for 12 hours.
In vitro, PSG12 significantly reduced oxidative stress, senescence, apoptosis, and inflammation in endothelial cells while preserving the extracellular matrix.
In vivo, PSG12 treatment reduced aortic rupture incidence and improved survival rates in a mouse model of TAD.

Conclusions:

PSG12 effectively restores endothelial cell homeostasis through multi-pathway synergistic modulation.
This GSH-responsive polymer represents a promising precision gas therapy platform for managing thoracic aortic dissection.
The developed polymer offers a controlled and targeted approach to H2S delivery for cardiovascular emergencies.