Authors
Zefeng Chen, Xianguan Yu, Leile Tang, Yunyue Zhao, Xubin Yang, Rongsheng Su, Zhaojun Xiong
Published in
Journal of cardiovascular pharmacology. Jul 06, 2026. Epub Jul 06, 2026.
Abstract
Fine particulate matter (PM2.5) is a pervasive air pollutant strongly linked to cardiovascular morbidity, yet effective countermeasures remain elusive. Here, we report that the natural triterpenoid asiatic acid (AA) protects against PM2.5-induced cardiotoxicity in male BALB/c mice by interrupting a mitochondrial DNA-driven pyroptotic cascade. Animals exposed to intranasal PM2.5 (16.2 mg kg-1, every 48 h for 21 days) developed cardiac hypertrophy, contractile dysfunction, extensive fibrosis and ultrastructural mitochondrial damage concomitant with cytosolic release of mtDNA fragments (CO1, ND1, Cytb), down-regulation of TFAM, and robust activation of cGAS-STING signalling (cGAS, STING, p-TBK1, p-IRF3). Downstream, NLRP3 inflammasome assembly, caspase-1 cleavage, GSDMD pore formation and maturation of IL-1β/IL-18 were markedly elevated. Oral administration of AA (12.5 or 25 mg kg-1 from day 7) dose-dependently restored TFAM expression, reduced cytosolic mtDNA, blunted cGAS-STING-NLRP3 axis activation, attenuated pyroptosis and preserved cardiac architecture and function. These findings identify mtDNA-triggered cGAS-STING-NLRP3 signalling as a critical pathway underlying PM2.5-elicited cardiomyocyte pyroptosis and establish AA as a promising therapeutic agent against air-pollution-associated cardiovascular injury.
PMID:
42407023
Bibliographic data and abstract were imported from PubMed on 07 Jul 2026.
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