Crosstalk of autophagy and ferroptosis in cardiovascular diseases: from pathophysiology to novel therapy
Cardiovascular diseases (CVDs) are characterized by high morbidity and mortality rates, imposing substantial epidemiological and economic burdens worldwide. Among the multifaceted mechanisms implicated in CVDs, autophagy and ferroptosis, two intimately linked cellular processes, emerge as pivotal pa...
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| Format: | Article |
| Language: | English |
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Elsevier
2025-07-01
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| Series: | Redox Biology |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2213231725002186 |
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| author | Changhao Hu Siying Gao Xinyi Li Kaiqing Yang Ye Cheng Wei Guo Huijun Wu Xueqin Cheng Weiwen Zhao Yuxuan Kong Haoyuan Hu Songyun Wang |
| author_facet | Changhao Hu Siying Gao Xinyi Li Kaiqing Yang Ye Cheng Wei Guo Huijun Wu Xueqin Cheng Weiwen Zhao Yuxuan Kong Haoyuan Hu Songyun Wang |
| author_sort | Changhao Hu |
| collection | DOAJ |
| description | Cardiovascular diseases (CVDs) are characterized by high morbidity and mortality rates, imposing substantial epidemiological and economic burdens worldwide. Among the multifaceted mechanisms implicated in CVDs, autophagy and ferroptosis, two intimately linked cellular processes, emerge as pivotal pathophysiological contributors. Autophagy, as an evolutionary conserved process that mediates the degradation and recycling of intracellular components, including proteins and organelles, exerts critical regulatory effects on iron metabolism and lipid homeostasis through various specialized forms, including ferritinophagy and lipophagy. Conversely, ferroptosis, an iron dependent form of cell death, involves oxidative stress and the accumulation of lipid peroxides, often triggered by iron overload and the dysfunction of glutathione peroxidase 4 (GPX4). The intricate crosstalk between these two processes, particularly ferritinophagy-mediated iron regulation influencing ferroptosis, plays a crucial role in diverse CVDs contexts. Key regulatory molecules, such as Beclin-1 and nuclear factor E2-related factor 2 (Nrf2), function as central hubs, orchestrating the intricate interplay between autophagy and ferroptosis. Through a comprehensive examination of these mechanisms across various CVDs pathologies, we summarize the latest findings and outline potential therapeutic strategies targeting the crosstalk between autophagy and ferroptosis. As the inaugural review focusing on autophagy-ferroptosis interactions in CVDs, this work significantly enriches our understanding of the pathophysiology of CVDs and identifies novel therapeutic targets with potential for precision medicine interventions in managing CVDs. |
| format | Article |
| id | doaj-art-c47c2933f7e54ab7b6b0c6d44d6d858d |
| institution | OA Journals |
| issn | 2213-2317 |
| language | English |
| publishDate | 2025-07-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Redox Biology |
| spelling | doaj-art-c47c2933f7e54ab7b6b0c6d44d6d858d2025-08-20T02:04:49ZengElsevierRedox Biology2213-23172025-07-018410370510.1016/j.redox.2025.103705Crosstalk of autophagy and ferroptosis in cardiovascular diseases: from pathophysiology to novel therapyChanghao Hu0Siying Gao1Xinyi Li2Kaiqing Yang3Ye Cheng4Wei Guo5Huijun Wu6Xueqin Cheng7Weiwen Zhao8Yuxuan Kong9Haoyuan Hu10Songyun Wang11Cardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCorresponding author.; Cardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCorresponding author.; Cardiovascular Hospital, Renmin Hospital of Wuhan University, Cardiac Autonomic Nervous System Research Center of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, ChinaCardiovascular diseases (CVDs) are characterized by high morbidity and mortality rates, imposing substantial epidemiological and economic burdens worldwide. Among the multifaceted mechanisms implicated in CVDs, autophagy and ferroptosis, two intimately linked cellular processes, emerge as pivotal pathophysiological contributors. Autophagy, as an evolutionary conserved process that mediates the degradation and recycling of intracellular components, including proteins and organelles, exerts critical regulatory effects on iron metabolism and lipid homeostasis through various specialized forms, including ferritinophagy and lipophagy. Conversely, ferroptosis, an iron dependent form of cell death, involves oxidative stress and the accumulation of lipid peroxides, often triggered by iron overload and the dysfunction of glutathione peroxidase 4 (GPX4). The intricate crosstalk between these two processes, particularly ferritinophagy-mediated iron regulation influencing ferroptosis, plays a crucial role in diverse CVDs contexts. Key regulatory molecules, such as Beclin-1 and nuclear factor E2-related factor 2 (Nrf2), function as central hubs, orchestrating the intricate interplay between autophagy and ferroptosis. Through a comprehensive examination of these mechanisms across various CVDs pathologies, we summarize the latest findings and outline potential therapeutic strategies targeting the crosstalk between autophagy and ferroptosis. As the inaugural review focusing on autophagy-ferroptosis interactions in CVDs, this work significantly enriches our understanding of the pathophysiology of CVDs and identifies novel therapeutic targets with potential for precision medicine interventions in managing CVDs.http://www.sciencedirect.com/science/article/pii/S2213231725002186AutophagyFerroptosisCardiovascular diseasesCrosstalkTherapeutic strategies |
| spellingShingle | Changhao Hu Siying Gao Xinyi Li Kaiqing Yang Ye Cheng Wei Guo Huijun Wu Xueqin Cheng Weiwen Zhao Yuxuan Kong Haoyuan Hu Songyun Wang Crosstalk of autophagy and ferroptosis in cardiovascular diseases: from pathophysiology to novel therapy Redox Biology Autophagy Ferroptosis Cardiovascular diseases Crosstalk Therapeutic strategies |
| title | Crosstalk of autophagy and ferroptosis in cardiovascular diseases: from pathophysiology to novel therapy |
| title_full | Crosstalk of autophagy and ferroptosis in cardiovascular diseases: from pathophysiology to novel therapy |
| title_fullStr | Crosstalk of autophagy and ferroptosis in cardiovascular diseases: from pathophysiology to novel therapy |
| title_full_unstemmed | Crosstalk of autophagy and ferroptosis in cardiovascular diseases: from pathophysiology to novel therapy |
| title_short | Crosstalk of autophagy and ferroptosis in cardiovascular diseases: from pathophysiology to novel therapy |
| title_sort | crosstalk of autophagy and ferroptosis in cardiovascular diseases from pathophysiology to novel therapy |
| topic | Autophagy Ferroptosis Cardiovascular diseases Crosstalk Therapeutic strategies |
| url | http://www.sciencedirect.com/science/article/pii/S2213231725002186 |
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