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research / researchmitochondrial ROS signaling in cancer

Navdeep S. Chandel

纳夫迪普·昌德尔

PhD

🏢Northwestern University Feinberg School of Medicine(西北大学费恩伯格医学院)🌐USA

David W. Cugell Professor of Medicine大卫·库格尔医学杰出教授

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Key Papers
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Awards
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Key Contributions

👥Biography 个人简介

Navdeep Chandel is a leading authority on mitochondrial reactive oxygen species (ROS) signaling and their role in cancer biology. His laboratory discovered that mitochondrial complex III-derived ROS are essential for HIF-1 activation under hypoxia, linking mitochondria to the hypoxic response central to tumor adaptation. Chandel has made seminal contributions to understanding how metformin inhibits complex I to alter cancer cell metabolism and how AMPK and mTOR integrate nutrient sensing with cell growth. His textbook on metabolism has become a standard reference for cancer metabolomics education.

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🧪Research Fields 研究领域

mitochondrial ROS线粒体活性氧
HIF-1 activationHIF-1激活
metformin cancer mechanism二甲双胍癌症机制
AMPK signalingAMPK信号传导
mTOR and metabolismmTOR与代谢

🎓Key Contributions 主要贡献

Mitochondrial ROS in HIF Activation

Discovered that mitochondrial complex III generates ROS essential for HIF-1 stabilization under hypoxia, establishing a fundamental mechanism linking mitochondrial function to the hypoxic tumor microenvironment.

Metformin Cancer Mechanism

Characterized metformin as an inhibitor of mitochondrial complex I that alters NADH/NAD ratio, reduces electron transport, and activates AMPK, clarifying its pleiotropic cancer-preventive and metabolic effects.

Representative Works 代表性著作

[1]

Mitochondrial Complex III ROS Regulate Cellular Oxygen Sensing

Science (2000)

Discovery of mitochondrial ROS as essential HIF-1 activating signal.

[2]

Metformin, Independent of AMPK, Inhibits mTORC1 in a RAG GTPase-Dependent Manner

Cell Metabolism (2011)

Mechanism of metformin in cancer cell metabolism.

🏆Awards & Recognition 奖项与荣誉

🏆American Society for Cell Biology Wilson Medal
🏆NCI Outstanding Investigator Award

📄Data Sources 数据来源

Last updated: 2026-01-15 | All information from publicly available academic sources

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