ArticleJournal of nanobiotechnology2026
Targeted inhibition of ATP synthase subunit c by pp10-loaded inhalable albumin nanoparticles ameliorates airway inflammation in asthma.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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16 authors.
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Abstract
The persistent opening of the mitochondrial permeability transition pore (mPTP) plays a critical role in bronchial asthma pathogenesis. The ATP synthase c subunit (c subunit) constitutes a core component of mPTP. A novel c subunit inhibitor, 1,3,8-triazaspiro [4.5] decane derivatives (PP10), effectively suppresses pathological mPTP opening without impairing ATP synthesis. Although intraperitoneal PP10 administration mitigates airway inflammation in asthmatic mice, its hydrophobicity hinders inhaled delivery to airway epithelial mitochondria, requiring penetration of the mucus layer, cell membrane, and mitochondrial outer membrane. To overcome this, we developed inhalable human serum albumin-triphenylphosphine-polyethylene glycol-PP10 nanoparticles (HSA-TPP-PEG-PP10 NPs). These NPs demonstrated efficient mucus penetration, high drug loading, mitochondria-targeting capability, and biosafety. They suppressed house dust mite/lipopolysaccharide (HDM/LPS)-induced mPTP opening, inhibited the mitochondrial DNA (mtDNA)-cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, reduced inflammation in human bronchial epithelial (HBE) cells, and alleviated airway inflammation in asthmatic mice upon inhalation.
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