Calcitonin Alleviates Sepsis-Induced Acute Lung Injury by Inhibiting the HMGB1/MyD88/NF-κB Pathway by Targeting CD3D
<i>CD3D</i> exacerbates sepsis-induced ALI by potentiating the HMGB1/MyD88/NF-κB pathway and NLRP3 inflammasome, driving inflammation and oxidative stress. Combined <i>CD3D</i> knockdown and calcitonin treatment offers a novel synergistic therapeutic strategy for mitigating pulmonary endothelial injury in sepsis.
Authors
- Ruiqing Zong (ORCID: https://orcid.org/0009-0004-3932-4026)
- Jun Jiang (ORCID: https://orcid.org/0009-0000-3404-2071)
- Hongyan Zhang (ORCID: https://orcid.org/0009-0003-5170-6660)
- Jian He (ORCID: https://orcid.org/0009-0003-3370-2295)
- Huiqi Wu (ORCID: https://orcid.org/0009-0005-1060-1672)
Institutions
- Fudan University (CN)
- Shanghai Changzheng Hospital (CN)
Publication Details
- Journal
- Frontiers in Bioscience-Landmark
- Published
- 2025-10-28
- DOI
- https://doi.org/10.31083/fbl44677
- Citations
- 1
- Primary Topic
- Advanced Glycation End Products research
- Type
- article
- Field-Weighted Citation Impact
- 1.32