Tangshenning Attenuates High Glucose-Induced Podocyte Injury via Restoring Autophagy Activity through Inhibiting mTORC1 Activation
Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus (DM) and the most common cause of death in diabetic patients. DN progression is associated with podocyte damage due to reduced autophagy caused by mTORC1 activation. Tangshenning (TSN) has been shown to reduce proteinuria...
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| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2022-01-01
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| Series: | Journal of Diabetes Research |
| Online Access: | http://dx.doi.org/10.1155/2022/1610416 |
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| _version_ | 1832552933866078208 |
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| author | Jiayi Xu Xiaomeng Shan Chunwei Chen Yanbin Gao Dawei Zou Xiaolei Wang Tao Wang Yimin Shi |
| author_facet | Jiayi Xu Xiaomeng Shan Chunwei Chen Yanbin Gao Dawei Zou Xiaolei Wang Tao Wang Yimin Shi |
| author_sort | Jiayi Xu |
| collection | DOAJ |
| description | Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus (DM) and the most common cause of death in diabetic patients. DN progression is associated with podocyte damage due to reduced autophagy caused by mTORC1 activation. Tangshenning (TSN) has been shown to reduce proteinuria, protect renal function, and reduce podocyte damage. Still, the effect of TSN on the autophagic activity of podocytes remains unclear. Herein, in vitro experiments using a high glucose-induced podocyte injury model were performed. Results showed that TSN treatment enhanced the weakened nephrin expression and autophagic activity of podocytes and inhibited the mTORC1 pathway (p-mTOR, mTOR, p-p70S6K, p70S6K, ULK1, and 4EBP1) under high glucose conditions. Furthermore, the mTORC1 activator (siRNA-TSC2) partially inhibited the above beneficial effects of TSN, suggesting that mTORC1 was the target of TSN to regulate autophagy. In summary, TSN reduces podocyte damage induced by high glucose via inhibiting mTORC1 pathway and downstream targets and restoring podocyte autophagy. |
| format | Article |
| id | doaj-art-a3a3d1634cdd4f448700b68640d8bb43 |
| institution | Kabale University |
| issn | 2314-6753 |
| language | English |
| publishDate | 2022-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Diabetes Research |
| spelling | doaj-art-a3a3d1634cdd4f448700b68640d8bb432025-02-03T05:57:28ZengWileyJournal of Diabetes Research2314-67532022-01-01202210.1155/2022/1610416Tangshenning Attenuates High Glucose-Induced Podocyte Injury via Restoring Autophagy Activity through Inhibiting mTORC1 ActivationJiayi Xu0Xiaomeng Shan1Chunwei Chen2Yanbin Gao3Dawei Zou4Xiaolei Wang5Tao Wang6Yimin Shi7School of Traditional Chinese MedicineSchool of Traditional Chinese MedicineSchool of Traditional Chinese MedicineSchool of Traditional Chinese MedicineSchool of Traditional Chinese MedicineSchool of Traditional Chinese MedicineSchool of Traditional Chinese MedicineSchool of Traditional Chinese MedicineDiabetic nephropathy (DN) is a microvascular complication of diabetes mellitus (DM) and the most common cause of death in diabetic patients. DN progression is associated with podocyte damage due to reduced autophagy caused by mTORC1 activation. Tangshenning (TSN) has been shown to reduce proteinuria, protect renal function, and reduce podocyte damage. Still, the effect of TSN on the autophagic activity of podocytes remains unclear. Herein, in vitro experiments using a high glucose-induced podocyte injury model were performed. Results showed that TSN treatment enhanced the weakened nephrin expression and autophagic activity of podocytes and inhibited the mTORC1 pathway (p-mTOR, mTOR, p-p70S6K, p70S6K, ULK1, and 4EBP1) under high glucose conditions. Furthermore, the mTORC1 activator (siRNA-TSC2) partially inhibited the above beneficial effects of TSN, suggesting that mTORC1 was the target of TSN to regulate autophagy. In summary, TSN reduces podocyte damage induced by high glucose via inhibiting mTORC1 pathway and downstream targets and restoring podocyte autophagy.http://dx.doi.org/10.1155/2022/1610416 |
| spellingShingle | Jiayi Xu Xiaomeng Shan Chunwei Chen Yanbin Gao Dawei Zou Xiaolei Wang Tao Wang Yimin Shi Tangshenning Attenuates High Glucose-Induced Podocyte Injury via Restoring Autophagy Activity through Inhibiting mTORC1 Activation Journal of Diabetes Research |
| title | Tangshenning Attenuates High Glucose-Induced Podocyte Injury via Restoring Autophagy Activity through Inhibiting mTORC1 Activation |
| title_full | Tangshenning Attenuates High Glucose-Induced Podocyte Injury via Restoring Autophagy Activity through Inhibiting mTORC1 Activation |
| title_fullStr | Tangshenning Attenuates High Glucose-Induced Podocyte Injury via Restoring Autophagy Activity through Inhibiting mTORC1 Activation |
| title_full_unstemmed | Tangshenning Attenuates High Glucose-Induced Podocyte Injury via Restoring Autophagy Activity through Inhibiting mTORC1 Activation |
| title_short | Tangshenning Attenuates High Glucose-Induced Podocyte Injury via Restoring Autophagy Activity through Inhibiting mTORC1 Activation |
| title_sort | tangshenning attenuates high glucose induced podocyte injury via restoring autophagy activity through inhibiting mtorc1 activation |
| url | http://dx.doi.org/10.1155/2022/1610416 |
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