Amplification of Endoplasmic Reticulum Stress via Inhibiting Lipid Droplet Formation to Enhance Chemodynamic Immunotherapy
to yield •OH accompanied by iLD release. •OH-triggered LPO of PUFAs not only causes cancer cell death, but also produces 4-HNE to provoke ER stress-mediated ICD. Intriguingly, iLD inhibits LDs formation and thereby reduces the sequestration of PUFAs as well as the recruitment of CRT by LDs, enabling improved chemodynamic immunotherapeutic efficacy. This study highlights a versatile strategy to enhance chemodynamic immunotherapy by modulating intracellular LDs.
Authors
- Lisen Lin (ORCID: https://orcid.org/0000-0003-4060-8881)
- Shanshan Peng (ORCID: https://orcid.org/0000-0001-8630-1725)
- Tingting Cui (ORCID: https://orcid.org/0009-0006-2560-7812)
- H G Huang
- Huilan Cai
- Xuegang Niu
- 杨黄浩
- Rujiang Ao
- Meili Yu
- Shaoru Zhuang
- Yu He
- Jun Wang
- Yang Zhu (ORCID: https://orcid.org/0000-0002-4747-9130)
Institutions
- Fujian Medical University (CN)
- First Affiliated Hospital of Fujian Medical University (CN)
- Fuzhou University (CN)
Publication Details
- Journal
- Advanced Science
- Published
- 2026-05-10
- DOI
- https://doi.org/10.1002/advs.75626
- Primary Topic
- Lipid metabolism and biosynthesis
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- National Natural Science Foundation of China