Mechanisms of Copper-Induced Autophagy and Links with Human Diseases

As a structural and catalytic cofactor, copper is involved in many biological pathways and is required for the biochemistry of all living organisms. However, excess intracellular copper can induce cell death due to its potential to catalyze the generation of reactive oxygen species, thus copper home...

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Main Authors: Yuanyuan Fu, Shuyan Zeng, Zhenlin Wang, Huiting Huang, Xin Zhao, Min Li
Format: Article
Language:English
Published: MDPI AG 2025-01-01
Series:Pharmaceuticals
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Online Access:https://www.mdpi.com/1424-8247/18/1/99
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author Yuanyuan Fu
Shuyan Zeng
Zhenlin Wang
Huiting Huang
Xin Zhao
Min Li
author_facet Yuanyuan Fu
Shuyan Zeng
Zhenlin Wang
Huiting Huang
Xin Zhao
Min Li
author_sort Yuanyuan Fu
collection DOAJ
description As a structural and catalytic cofactor, copper is involved in many biological pathways and is required for the biochemistry of all living organisms. However, excess intracellular copper can induce cell death due to its potential to catalyze the generation of reactive oxygen species, thus copper homeostasis is strictly regulated. And the deficiency or accumulation of intracellular copper is connected with various pathological conditions. Since the success of platinum-based compounds in the clinical treatment of various types of neoplasias, metal-based drugs have shown encouraging perspectives for drug development. Compared to platinum, copper is an essential intracellular trace element that may have better prospects for drug development than platinum. Recently, the potential therapeutic role of copper-induced autophagy in chronic diseases such as Parkinson’s, Wilson’s, and cardiovascular disease has already been demonstrated. In brief, copper ions, numerous copper complexes, and copper-based nano-preparations could induce autophagy, a lysosome-dependent process that plays an important role in various human diseases. In this review, we not only focus on the current advances in elucidating the mechanisms of copper or copper-based compounds/preparations on the regulation of autophagy but also outline the association between copper-induced autophagy and human diseases.
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spelling doaj-art-f27c93808cb74ea482ae8345c314a67b2025-01-24T13:45:23ZengMDPI AGPharmaceuticals1424-82472025-01-011819910.3390/ph18010099Mechanisms of Copper-Induced Autophagy and Links with Human DiseasesYuanyuan Fu0Shuyan Zeng1Zhenlin Wang2Huiting Huang3Xin Zhao4Min Li5Guangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, The NMPA and the State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou 511436, ChinaGuangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, The NMPA and the State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou 511436, ChinaGuangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, The NMPA and the State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou 511436, ChinaGuangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, The NMPA and the State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou 511436, ChinaGuangzhou Municipal and Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, The NMPA and the State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou 511436, ChinaSchool of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou 510006, ChinaAs a structural and catalytic cofactor, copper is involved in many biological pathways and is required for the biochemistry of all living organisms. However, excess intracellular copper can induce cell death due to its potential to catalyze the generation of reactive oxygen species, thus copper homeostasis is strictly regulated. And the deficiency or accumulation of intracellular copper is connected with various pathological conditions. Since the success of platinum-based compounds in the clinical treatment of various types of neoplasias, metal-based drugs have shown encouraging perspectives for drug development. Compared to platinum, copper is an essential intracellular trace element that may have better prospects for drug development than platinum. Recently, the potential therapeutic role of copper-induced autophagy in chronic diseases such as Parkinson’s, Wilson’s, and cardiovascular disease has already been demonstrated. In brief, copper ions, numerous copper complexes, and copper-based nano-preparations could induce autophagy, a lysosome-dependent process that plays an important role in various human diseases. In this review, we not only focus on the current advances in elucidating the mechanisms of copper or copper-based compounds/preparations on the regulation of autophagy but also outline the association between copper-induced autophagy and human diseases.https://www.mdpi.com/1424-8247/18/1/99autophagycoppercopper-based agentshuman diseasestherapeutic potential
spellingShingle Yuanyuan Fu
Shuyan Zeng
Zhenlin Wang
Huiting Huang
Xin Zhao
Min Li
Mechanisms of Copper-Induced Autophagy and Links with Human Diseases
Pharmaceuticals
autophagy
copper
copper-based agents
human diseases
therapeutic potential
title Mechanisms of Copper-Induced Autophagy and Links with Human Diseases
title_full Mechanisms of Copper-Induced Autophagy and Links with Human Diseases
title_fullStr Mechanisms of Copper-Induced Autophagy and Links with Human Diseases
title_full_unstemmed Mechanisms of Copper-Induced Autophagy and Links with Human Diseases
title_short Mechanisms of Copper-Induced Autophagy and Links with Human Diseases
title_sort mechanisms of copper induced autophagy and links with human diseases
topic autophagy
copper
copper-based agents
human diseases
therapeutic potential
url https://www.mdpi.com/1424-8247/18/1/99
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AT shuyanzeng mechanismsofcopperinducedautophagyandlinkswithhumandiseases
AT zhenlinwang mechanismsofcopperinducedautophagyandlinkswithhumandiseases
AT huitinghuang mechanismsofcopperinducedautophagyandlinkswithhumandiseases
AT xinzhao mechanismsofcopperinducedautophagyandlinkswithhumandiseases
AT minli mechanismsofcopperinducedautophagyandlinkswithhumandiseases