Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injury
Abstract Ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury (AKI). The kidney is susceptible to IRI under several clinical conditions, including hypotension, sepsis, and surgical procedures, such as partial nephrectomy and kidney transplantation. Extensive research has been c...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Nature Publishing Group
2024-02-01
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| Series: | Cell Death Discovery |
| Online Access: | https://doi.org/10.1038/s41420-024-01843-5 |
| _version_ | 1797275861283504128 |
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| author | Yongming Chen Zixian Li Hongyong Zhang Huixia Chen Junfeng Hao Huafeng Liu Xiaoyu Li |
| author_facet | Yongming Chen Zixian Li Hongyong Zhang Huixia Chen Junfeng Hao Huafeng Liu Xiaoyu Li |
| author_sort | Yongming Chen |
| collection | DOAJ |
| description | Abstract Ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury (AKI). The kidney is susceptible to IRI under several clinical conditions, including hypotension, sepsis, and surgical procedures, such as partial nephrectomy and kidney transplantation. Extensive research has been conducted on the mechanism and intervention strategies of renal IRI in past decades; however, the complex pathophysiology of IRI-induced AKI (IRI-AKI) is not fully understood, and there remains a lack of effective treatments for AKI. Renal IRI involves several processes, including reactive oxygen species (ROS) production, inflammation, and apoptosis. Mitochondria, the centers of energy metabolism, are increasingly recognized as substantial contributors to the early phases of IRI. Multiple mitochondrial lesions have been observed in the renal tubular epithelial cells (TECs) of IRI-AKI mice, and damaged or dysfunctional mitochondria are toxic to the cells because they produce ROS and release cell death factors, resulting in TEC apoptosis. In this review, we summarize the recent advances in the mitochondrial pathology in ischemic AKI and highlight promising therapeutic approaches targeting mitochondrial dysfunction to prevent or treat human ischemic AKI. |
| first_indexed | 2024-03-07T15:20:06Z |
| format | Article |
| id | doaj.art-8e012b9792ae4e96b8ecba67a43c3bec |
| institution | Directory Open Access Journal |
| issn | 2058-7716 |
| language | English |
| last_indexed | 2024-03-07T15:20:06Z |
| publishDate | 2024-02-01 |
| publisher | Nature Publishing Group |
| record_format | Article |
| series | Cell Death Discovery |
| spelling | doaj.art-8e012b9792ae4e96b8ecba67a43c3bec2024-03-05T17:41:46ZengNature Publishing GroupCell Death Discovery2058-77162024-02-0110111110.1038/s41420-024-01843-5Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injuryYongming Chen0Zixian Li1Hongyong Zhang2Huixia Chen3Junfeng Hao4Huafeng Liu5Xiaoyu Li6Institute of Nephrology, and Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases, Affiliated Hospital of Guangdong Medical UniversityInstitute of Nephrology, and Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases, Affiliated Hospital of Guangdong Medical UniversityZhanjiang Institute of Clinical Medicine, Central People’s Hospital of Zhanjiang, Guangdong Medical University Zhan-jiang Central HospitalInstitute of Nephrology, and Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases, Affiliated Hospital of Guangdong Medical UniversityInstitute of Nephrology, and Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases, Affiliated Hospital of Guangdong Medical UniversityInstitute of Nephrology, and Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases, Affiliated Hospital of Guangdong Medical UniversityInstitute of Nephrology, and Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-Communicable Diseases, Affiliated Hospital of Guangdong Medical UniversityAbstract Ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury (AKI). The kidney is susceptible to IRI under several clinical conditions, including hypotension, sepsis, and surgical procedures, such as partial nephrectomy and kidney transplantation. Extensive research has been conducted on the mechanism and intervention strategies of renal IRI in past decades; however, the complex pathophysiology of IRI-induced AKI (IRI-AKI) is not fully understood, and there remains a lack of effective treatments for AKI. Renal IRI involves several processes, including reactive oxygen species (ROS) production, inflammation, and apoptosis. Mitochondria, the centers of energy metabolism, are increasingly recognized as substantial contributors to the early phases of IRI. Multiple mitochondrial lesions have been observed in the renal tubular epithelial cells (TECs) of IRI-AKI mice, and damaged or dysfunctional mitochondria are toxic to the cells because they produce ROS and release cell death factors, resulting in TEC apoptosis. In this review, we summarize the recent advances in the mitochondrial pathology in ischemic AKI and highlight promising therapeutic approaches targeting mitochondrial dysfunction to prevent or treat human ischemic AKI.https://doi.org/10.1038/s41420-024-01843-5 |
| spellingShingle | Yongming Chen Zixian Li Hongyong Zhang Huixia Chen Junfeng Hao Huafeng Liu Xiaoyu Li Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injury Cell Death Discovery |
| title | Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injury |
| title_full | Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injury |
| title_fullStr | Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injury |
| title_full_unstemmed | Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injury |
| title_short | Mitochondrial metabolism and targeted treatment strategies in ischemic-induced acute kidney injury |
| title_sort | mitochondrial metabolism and targeted treatment strategies in ischemic induced acute kidney injury |
| url | https://doi.org/10.1038/s41420-024-01843-5 |
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