Progress of Chinese Herbal Medicines Intervening in Acute Respiratory Distress Syndrome Through Multiple Mechanisms
Acute respiratory distress syndrome (ARDS) is a critical pulmonary disorder triggered by multiple factors, with pathological mechanisms involving inflammatory storms, oxidative stress, alveolar-endothelial barrier disruption, and multiple cell death modalities (eg, pyroptosis and ferroptosis). Chinese herbal medicines(CHMs) and their active components have demonstrated their unique potential in the intervention of ARDS through multiple targets and multiple pathways approaches: (1) inhibiting the Wnt/β-catenin signaling pathway to mitigate inflammation; (2) regulating macrophage M1/M2 polarization; (3) activating the Sirtuin-3 (SIRT3) pathway to alleviate oxidative damage; (4) suppressing NLRP3 inflammasome-mediated pyroptosis; (5) improving barrier function via inhibition of the PI3K/AKT signaling pathway;(6) inhibiting ferroptosis through modulation of the Nrf2/SLC7A11/GPX4 axis. In the future, we can start from the pathogenesis of ARDS, and based on the efficacy and results of traditional Chinese medicine and its active components in regulating related signaling pathways to intervene in ARDS, provide references for the research and development of new drugs and clinical applications.
Authors
- Yaqing Zhou (ORCID: https://orcid.org/0000-0003-1887-872X)
- Ying Wang (ORCID: https://orcid.org/0000-0001-8537-3954)
- Jingjing Ren (ORCID: https://orcid.org/0000-0003-2582-659X)
- Xuehua Pu
Institutions
- Nanjing University of Chinese Medicine (CN)
- Nantong University (CN)
- Second People's Hospital of NanTong (CN)
- The Affiliated Taizhou People's Hospital of Nanjing Medical University (CN)
- Anyang Hospital of Traditional Chinese Medicine (CN)
- Nanjing Medical University (CN)
Publication Details
- Journal
- Natural Product Communications
- Published
- 2025-09-01
- DOI
- https://doi.org/10.1177/1934578x251375568
- Primary Topic
- Inflammasome and immune disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00