Cellular senescence of renal tubular epithelial cells in acute kidney injury
Abstract Cellular senescence represents an irreversible state of cell-cycle arrest during which cells secrete senescence-associated secretory phenotypes, including inflammatory factors and chemokines. Additionally, these cells exhibit an apoptotic resistance phenotype. Cellular senescence serves a p...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Nature Publishing Group
2024-02-01
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| Series: | Cell Death Discovery |
| Online Access: | https://doi.org/10.1038/s41420-024-01831-9 |
| _version_ | 1797275848724709376 |
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| author | Juan Chen Huhai Zhang Xiangling Yi Qian Dou Xin Yang Yani He Jia Chen Kehong Chen |
| author_facet | Juan Chen Huhai Zhang Xiangling Yi Qian Dou Xin Yang Yani He Jia Chen Kehong Chen |
| author_sort | Juan Chen |
| collection | DOAJ |
| description | Abstract Cellular senescence represents an irreversible state of cell-cycle arrest during which cells secrete senescence-associated secretory phenotypes, including inflammatory factors and chemokines. Additionally, these cells exhibit an apoptotic resistance phenotype. Cellular senescence serves a pivotal role not only in embryonic development, tissue regeneration, and tumor suppression but also in the pathogenesis of age-related degenerative diseases, malignancies, metabolic diseases, and kidney diseases. The senescence of renal tubular epithelial cells (RTEC) constitutes a critical cellular event in the progression of acute kidney injury (AKI). RTEC senescence inhibits renal regeneration and repair processes and, concurrently, promotes the transition of AKI to chronic kidney disease via the senescence-associated secretory phenotype. The mechanisms underlying cellular senescence are multifaceted and include telomere shortening or damage, DNA damage, mitochondrial autophagy deficiency, cellular metabolic disorders, endoplasmic reticulum stress, and epigenetic regulation. Strategies aimed at inhibiting RTEC senescence, targeting the clearance of senescent RTEC, or promoting the apoptosis of senescent RTEC hold promise for enhancing the renal prognosis of AKI. This review primarily focuses on the characteristics and mechanisms of RTEC senescence, and the impact of intervening RTEC senescence on the prognosis of AKI, aiming to provide a foundation for understanding the pathogenesis and providing potentially effective approaches for AKI treatment. |
| first_indexed | 2024-03-07T15:19:55Z |
| format | Article |
| id | doaj.art-5e2437e641ed4307b685501d1634de06 |
| institution | Directory Open Access Journal |
| issn | 2058-7716 |
| language | English |
| last_indexed | 2024-03-07T15:19:55Z |
| publishDate | 2024-02-01 |
| publisher | Nature Publishing Group |
| record_format | Article |
| series | Cell Death Discovery |
| spelling | doaj.art-5e2437e641ed4307b685501d1634de062024-03-05T17:41:48ZengNature Publishing GroupCell Death Discovery2058-77162024-02-0110111310.1038/s41420-024-01831-9Cellular senescence of renal tubular epithelial cells in acute kidney injuryJuan Chen0Huhai Zhang1Xiangling Yi2Qian Dou3Xin Yang4Yani He5Jia Chen6Kehong Chen7Department of Nephrology, Daping Hospital, Army Medical UniversityDepartment of Nephrology, Southwest Hospital, Army Medical UniversityDepartment of Nephrology, Daping Hospital, Army Medical UniversityDepartment of Nephrology, Daping Hospital, Army Medical UniversityDepartment of Nephrology, Daping Hospital, Army Medical UniversityDepartment of Nephrology, Daping Hospital, Army Medical UniversityDepartment of Nephrology, Daping Hospital, Army Medical UniversityDepartment of Nephrology, Daping Hospital, Army Medical UniversityAbstract Cellular senescence represents an irreversible state of cell-cycle arrest during which cells secrete senescence-associated secretory phenotypes, including inflammatory factors and chemokines. Additionally, these cells exhibit an apoptotic resistance phenotype. Cellular senescence serves a pivotal role not only in embryonic development, tissue regeneration, and tumor suppression but also in the pathogenesis of age-related degenerative diseases, malignancies, metabolic diseases, and kidney diseases. The senescence of renal tubular epithelial cells (RTEC) constitutes a critical cellular event in the progression of acute kidney injury (AKI). RTEC senescence inhibits renal regeneration and repair processes and, concurrently, promotes the transition of AKI to chronic kidney disease via the senescence-associated secretory phenotype. The mechanisms underlying cellular senescence are multifaceted and include telomere shortening or damage, DNA damage, mitochondrial autophagy deficiency, cellular metabolic disorders, endoplasmic reticulum stress, and epigenetic regulation. Strategies aimed at inhibiting RTEC senescence, targeting the clearance of senescent RTEC, or promoting the apoptosis of senescent RTEC hold promise for enhancing the renal prognosis of AKI. This review primarily focuses on the characteristics and mechanisms of RTEC senescence, and the impact of intervening RTEC senescence on the prognosis of AKI, aiming to provide a foundation for understanding the pathogenesis and providing potentially effective approaches for AKI treatment.https://doi.org/10.1038/s41420-024-01831-9 |
| spellingShingle | Juan Chen Huhai Zhang Xiangling Yi Qian Dou Xin Yang Yani He Jia Chen Kehong Chen Cellular senescence of renal tubular epithelial cells in acute kidney injury Cell Death Discovery |
| title | Cellular senescence of renal tubular epithelial cells in acute kidney injury |
| title_full | Cellular senescence of renal tubular epithelial cells in acute kidney injury |
| title_fullStr | Cellular senescence of renal tubular epithelial cells in acute kidney injury |
| title_full_unstemmed | Cellular senescence of renal tubular epithelial cells in acute kidney injury |
| title_short | Cellular senescence of renal tubular epithelial cells in acute kidney injury |
| title_sort | cellular senescence of renal tubular epithelial cells in acute kidney injury |
| url | https://doi.org/10.1038/s41420-024-01831-9 |
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