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Updated: May 31, 2026

Positron Emission Tomography Using 64-Copper as a Tracer for the Study of Copper-Related Disorders
Published on: April 28, 2023
Copper and cuproptosis: mechanisms, biology, and roles in disease
Fudi Wang1, WenYe Liu2, Cong Tao3
1The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine, Hangzhou 310058, China; The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China; Global Innovation Institute of Element Science (GIIES-JLU), The First Hospital of Jilin University, Changchun 130021, China.
Abstract:
Copper, an evolutionarily conserved redox-active trace element, serves as an irreplaceable core pillar of eukaryotic life-orchestrating cuproenzyme catalysis, metabolic signaling networks, and organelle homeostasis across molecule-to-organism scales. Its strict homeostasis is a prerequisite for physiological function, and its dysregulation is a hallmark of diverse pathologies. The discovery of cuproptosis-a distinct mitochondria-centric programmed cell death-has fundamentally upended traditional paradigms of metal-mediated cytotoxicity. Cuprology, serves as an integrative interdisciplinary framework to unify copper's spatiotemporal regulation across biological hierarchies. This inherent duality governs health and disease: physiological copper sustains developmental metabolism and redox balance, while deficiency or overload drives pathogenesis spanning metabolic disorders, neurodegeneration, and cancer. Integrating foundational mechanistic insights with cutting-edge translational breakthroughs-from copper ionophores to nano-carrier-mediated precision delivery. This review synthesizes the intricate crosstalk between copper homeostasis, cuproptosis circuitry, and cellular metabolism under the Cuprology framework. It further charts a clear roadmap for targeting copper-cuproptosis axes, unlocking transformative therapeutic strategies for recalcitrant diseases and steering a new era of research into cell death and metabolic regulation.
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