Inhibition of Lactate Accumulation via USP38‐Mediated MCT1 Deubiquitination Activates AKT/mTOR Signaling to Mitigate PM2.5‐Induced Lung Injury
USP38 reduces lactate accumulation by promoting AKT/mTOR pathway activation through MCT1-mediated lactate export, thereby alleviating PM2.5-induced lung injury. These findings reveal a novel mechanism of PM2.5-related lung injury and highlight potential therapeutic targets.
Authors
- Xixin Yan (ORCID: https://orcid.org/0009-0001-7490-8762)
- Zixiao Chen
- Lingshan Chao
- Jing Li (ORCID: https://orcid.org/0000-0002-5848-2781)
- Zhongxiao Jia (ORCID: https://orcid.org/0000-0001-9761-8517)
- Jialun Chen (ORCID: https://orcid.org/0000-0002-6447-5713)
- Siqin Han
- Jing Cao (ORCID: https://orcid.org/0009-0000-2161-8385)
- Shujie Hou
Institutions
- Hebei Medical University (CN)
- Second Hospital of Hebei Medical University (CN)
Publication Details
- Journal
- Journal of Clinical Laboratory Analysis
- Published
- 2025-04-01
- DOI
- https://doi.org/10.1002/jcla.70028
- Citations
- 2
- Primary Topic
- Mitochondrial Function and Pathology
- Type
- article
- Field-Weighted Citation Impact
- 1.61
Funders
- National Natural Science Foundation of China
- Natural Science Foundation of Hebei Province