Podocyte senescence: from molecular mechanisms to therapeutics
As an important component of the glomerular filtration membrane, the state of the podocytes is closely related to kidney function, they are also key cells involved in aging and play a central role in the damage caused by renal aging. Therefore, understanding the aging process of podocytes will allow...
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2024-12-01
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| Series: | Renal Failure |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/0886022X.2024.2398712 |
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| author | Qian Zhao Yongzhang Huang Ningying Fu Caixia Cui Xuan Peng Haiyan Kang Jie Xiao Guibao Ke |
| author_facet | Qian Zhao Yongzhang Huang Ningying Fu Caixia Cui Xuan Peng Haiyan Kang Jie Xiao Guibao Ke |
| author_sort | Qian Zhao |
| collection | DOAJ |
| description | As an important component of the glomerular filtration membrane, the state of the podocytes is closely related to kidney function, they are also key cells involved in aging and play a central role in the damage caused by renal aging. Therefore, understanding the aging process of podocytes will allow us to understand their susceptibility to injury and identify targeted protective mechanisms. In fact, the process of physiological aging itself can induce podocyte senescence. Pathological stresses, such as oxidative stress, mitochondrial damage, secretion of senescence-associated secretory phenotype, reduced autophagy, oncogene activation, altered transcription factors, DNA damage response, and other factors, play a crucial role in inducing premature senescence and accelerating aging. Senescence-associated-β-galactosidase (SA-β-gal) is a marker of aging, and β-hydroxybutyric acid treatment can reduce SA-β-gal activity to alleviate cellular senescence and damage. In addition, CCAAT/enhancer-binding protein-α, transforming growth factor-β signaling, glycogen synthase kinase-3β, cycle-dependent kinase, programmed cell death protein 1, and plasminogen activator inhibitor-1 are closely related to aging. The absence or elevation of these factors can affect aging through different mechanisms. Podocyte injury is not an independent process, and injured podocytes interact with the surrounding epithelial cells or other kidney cells to mediate the injury or loss of podocytes. In this review, we discuss the manifestations, molecular mechanisms, biomarkers, and therapeutic drugs for podocyte senescence. We included elamipretide, lithium, calorie restriction, rapamycin; and emerging treatment strategies, such as gene and immune therapies. More importantly, we summarize how podocyte interact with other kidney cells. |
| format | Article |
| id | doaj-art-ef71fad370d84b5e9a0202dd2b1ffcc2 |
| institution | DOAJ |
| issn | 0886-022X 1525-6049 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Renal Failure |
| spelling | doaj-art-ef71fad370d84b5e9a0202dd2b1ffcc22025-08-20T03:05:26ZengTaylor & Francis GroupRenal Failure0886-022X1525-60492024-12-0146210.1080/0886022X.2024.2398712Podocyte senescence: from molecular mechanisms to therapeuticsQian Zhao0Yongzhang Huang1Ningying Fu2Caixia Cui3Xuan Peng4Haiyan Kang5Jie Xiao6Guibao Ke7Department of Nephrology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, ChinaDepartment of Nephrology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, ChinaDepartment of Nephrology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, ChinaDepartment of Nephrology, The First Affiliated Hospital of Bengbu Medical University, Bengbu, ChinaDepartment of Nephrology, Affiliated Hospital/Clinical Medical College of Chengdu University, Chengdu, ChinaDepartment of Nephrology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, ChinaDepartment of Nephrology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, ChinaDepartment of Nephrology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, ChinaAs an important component of the glomerular filtration membrane, the state of the podocytes is closely related to kidney function, they are also key cells involved in aging and play a central role in the damage caused by renal aging. Therefore, understanding the aging process of podocytes will allow us to understand their susceptibility to injury and identify targeted protective mechanisms. In fact, the process of physiological aging itself can induce podocyte senescence. Pathological stresses, such as oxidative stress, mitochondrial damage, secretion of senescence-associated secretory phenotype, reduced autophagy, oncogene activation, altered transcription factors, DNA damage response, and other factors, play a crucial role in inducing premature senescence and accelerating aging. Senescence-associated-β-galactosidase (SA-β-gal) is a marker of aging, and β-hydroxybutyric acid treatment can reduce SA-β-gal activity to alleviate cellular senescence and damage. In addition, CCAAT/enhancer-binding protein-α, transforming growth factor-β signaling, glycogen synthase kinase-3β, cycle-dependent kinase, programmed cell death protein 1, and plasminogen activator inhibitor-1 are closely related to aging. The absence or elevation of these factors can affect aging through different mechanisms. Podocyte injury is not an independent process, and injured podocytes interact with the surrounding epithelial cells or other kidney cells to mediate the injury or loss of podocytes. In this review, we discuss the manifestations, molecular mechanisms, biomarkers, and therapeutic drugs for podocyte senescence. We included elamipretide, lithium, calorie restriction, rapamycin; and emerging treatment strategies, such as gene and immune therapies. More importantly, we summarize how podocyte interact with other kidney cells.https://www.tandfonline.com/doi/10.1080/0886022X.2024.2398712Podocyte senescencemolecular mechanismsbiomarkersintervention targets |
| spellingShingle | Qian Zhao Yongzhang Huang Ningying Fu Caixia Cui Xuan Peng Haiyan Kang Jie Xiao Guibao Ke Podocyte senescence: from molecular mechanisms to therapeutics Renal Failure Podocyte senescence molecular mechanisms biomarkers intervention targets |
| title | Podocyte senescence: from molecular mechanisms to therapeutics |
| title_full | Podocyte senescence: from molecular mechanisms to therapeutics |
| title_fullStr | Podocyte senescence: from molecular mechanisms to therapeutics |
| title_full_unstemmed | Podocyte senescence: from molecular mechanisms to therapeutics |
| title_short | Podocyte senescence: from molecular mechanisms to therapeutics |
| title_sort | podocyte senescence from molecular mechanisms to therapeutics |
| topic | Podocyte senescence molecular mechanisms biomarkers intervention targets |
| url | https://www.tandfonline.com/doi/10.1080/0886022X.2024.2398712 |
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