Dual-responsive nanoparticles targeting ACE-II senescence for therapeutic mitigation of acute lung injury

Abstract Acute lung injury (ALI) is a life-threatening condition characterized by severe pulmonary dysfunction, with alveolar type II epithelial cell (ACE-II) senescence playing a pivotal role in its progression. In this study, we developed pH/reactive oxygen species (ROS) dual-responsive nanopartic...

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Main Authors: Linlin Gao, Fushuang Zheng, Zhiling Fu, Wei Wang
Format: Article
Language:English
Published: BMC 2025-05-01
Series:Journal of Nanobiotechnology
Subjects:
Online Access:https://doi.org/10.1186/s12951-025-03382-2
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author Linlin Gao
Fushuang Zheng
Zhiling Fu
Wei Wang
author_facet Linlin Gao
Fushuang Zheng
Zhiling Fu
Wei Wang
author_sort Linlin Gao
collection DOAJ
description Abstract Acute lung injury (ALI) is a life-threatening condition characterized by severe pulmonary dysfunction, with alveolar type II epithelial cell (ACE-II) senescence playing a pivotal role in its progression. In this study, we developed pH/reactive oxygen species (ROS) dual-responsive nanoparticles (GNPsanti-SP-C) for the targeted delivery of Growth Differentiation Factor 15 (GDF15) to counteract ACE-II senescence. These nanoparticles (NPs) effectively activate the AMP-activated protein kinase (AMPK)/Sirtuin 1 (SIRT1) signaling pathway, inducing the mitochondrial unfolded protein response (UPRmt) and reversing senescence-associated cellular dysfunction. GNPsanti-SP-C were systematically engineered and demonstrated robust pH/ROS sensitivity, efficient GDF15 release, and precise ACE-II targeting. In lipopolysaccharide (LPS)-induced ALI mouse model, GNPsanti-SP-C treatment significantly mitigated lung injury, reduced inflammatory responses, and enhanced pulmonary function, as evidenced by decreased inflammatory markers, lung edema, and improved histopathology. Single-cell transcriptomic and proteomic analyses revealed increased ACE-II cell populations, reduced expression of senescence markers, and upregulation of AMPK/SIRT1 signaling. In vitro studies further demonstrated that UPRmt activation is associated with the NPs’ therapeutic effects, suggesting a potential role in their mechanism of action. These findings demonstrate the potential of GDF15-loaded dual-responsive NPs as an innovative strategy to address cellular senescence and alleviate ALI-associated pulmonary damage. Graphical abstract
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spelling doaj-art-7aa642ab3eec4c9a8e097c677d7568232025-08-20T03:53:13ZengBMCJournal of Nanobiotechnology1477-31552025-05-0123112510.1186/s12951-025-03382-2Dual-responsive nanoparticles targeting ACE-II senescence for therapeutic mitigation of acute lung injuryLinlin Gao0Fushuang Zheng1Zhiling Fu2Wei Wang3Department of Critical Care Medicine, Shengjing Hospital of China Medical UniversityDepartment of Thoracic Surgery, Shengjing Hospital of China Medical UniversityDepartment of Anesthesiology, Shengjing Hospital of China Medical UniversityDepartment of Anesthesiology, Shengjing Hospital of China Medical UniversityAbstract Acute lung injury (ALI) is a life-threatening condition characterized by severe pulmonary dysfunction, with alveolar type II epithelial cell (ACE-II) senescence playing a pivotal role in its progression. In this study, we developed pH/reactive oxygen species (ROS) dual-responsive nanoparticles (GNPsanti-SP-C) for the targeted delivery of Growth Differentiation Factor 15 (GDF15) to counteract ACE-II senescence. These nanoparticles (NPs) effectively activate the AMP-activated protein kinase (AMPK)/Sirtuin 1 (SIRT1) signaling pathway, inducing the mitochondrial unfolded protein response (UPRmt) and reversing senescence-associated cellular dysfunction. GNPsanti-SP-C were systematically engineered and demonstrated robust pH/ROS sensitivity, efficient GDF15 release, and precise ACE-II targeting. In lipopolysaccharide (LPS)-induced ALI mouse model, GNPsanti-SP-C treatment significantly mitigated lung injury, reduced inflammatory responses, and enhanced pulmonary function, as evidenced by decreased inflammatory markers, lung edema, and improved histopathology. Single-cell transcriptomic and proteomic analyses revealed increased ACE-II cell populations, reduced expression of senescence markers, and upregulation of AMPK/SIRT1 signaling. In vitro studies further demonstrated that UPRmt activation is associated with the NPs’ therapeutic effects, suggesting a potential role in their mechanism of action. These findings demonstrate the potential of GDF15-loaded dual-responsive NPs as an innovative strategy to address cellular senescence and alleviate ALI-associated pulmonary damage. Graphical abstracthttps://doi.org/10.1186/s12951-025-03382-2Acute lung injuryNanoparticle therapyGDF15Cellular senescenceAMPK/SIRT1 signalingMitochondrial unfolded protein response
spellingShingle Linlin Gao
Fushuang Zheng
Zhiling Fu
Wei Wang
Dual-responsive nanoparticles targeting ACE-II senescence for therapeutic mitigation of acute lung injury
Journal of Nanobiotechnology
Acute lung injury
Nanoparticle therapy
GDF15
Cellular senescence
AMPK/SIRT1 signaling
Mitochondrial unfolded protein response
title Dual-responsive nanoparticles targeting ACE-II senescence for therapeutic mitigation of acute lung injury
title_full Dual-responsive nanoparticles targeting ACE-II senescence for therapeutic mitigation of acute lung injury
title_fullStr Dual-responsive nanoparticles targeting ACE-II senescence for therapeutic mitigation of acute lung injury
title_full_unstemmed Dual-responsive nanoparticles targeting ACE-II senescence for therapeutic mitigation of acute lung injury
title_short Dual-responsive nanoparticles targeting ACE-II senescence for therapeutic mitigation of acute lung injury
title_sort dual responsive nanoparticles targeting ace ii senescence for therapeutic mitigation of acute lung injury
topic Acute lung injury
Nanoparticle therapy
GDF15
Cellular senescence
AMPK/SIRT1 signaling
Mitochondrial unfolded protein response
url https://doi.org/10.1186/s12951-025-03382-2
work_keys_str_mv AT linlingao dualresponsivenanoparticlestargetingaceiisenescencefortherapeuticmitigationofacutelunginjury
AT fushuangzheng dualresponsivenanoparticlestargetingaceiisenescencefortherapeuticmitigationofacutelunginjury
AT zhilingfu dualresponsivenanoparticlestargetingaceiisenescencefortherapeuticmitigationofacutelunginjury
AT weiwang dualresponsivenanoparticlestargetingaceiisenescencefortherapeuticmitigationofacutelunginjury