Cordycepin ameliorates diabetic nephropathy injury by activating the SLC7A11/GPX4 pathway

ABSTRACT Background Cordycepin (CRD) has been identified to alleviate diabetes‐induced injuries and complications including diabetic nephropathy (DN). Here, this work focused on probing the specific effects and potential mechanisms of CRD on DN progression. Methods High glucose (HG)‐induced mouse po...

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Main Authors: Bing Wu, Jing Wang, Xiaohui Yan, Gang Jin, Qiong Wang
Format: Article
Language:English
Published: Wiley 2025-06-01
Series:Journal of Diabetes Investigation
Subjects:
Online Access:https://doi.org/10.1111/jdi.14407
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author Bing Wu
Jing Wang
Xiaohui Yan
Gang Jin
Qiong Wang
author_facet Bing Wu
Jing Wang
Xiaohui Yan
Gang Jin
Qiong Wang
author_sort Bing Wu
collection DOAJ
description ABSTRACT Background Cordycepin (CRD) has been identified to alleviate diabetes‐induced injuries and complications including diabetic nephropathy (DN). Here, this work focused on probing the specific effects and potential mechanisms of CRD on DN progression. Methods High glucose (HG)‐induced mouse podocyte cell line (MPC5) was used for in vitro functional analyses. Cell proliferation and apoptosis were determined using cell counting kit‐8 assay, 5‐ethynyl‐2′‐deoxyuridine assay, and flow cytometry, respectively. ELISA analysis detected inflammatory factors. Cell ferroptosis was assessed by measuring the levels of Fe2+, glutathione, reactive oxygen species, and malonaldehyde. Results CRD treatment suppressed HG‐induced apoptosis, inflammation, and ferroptosis in podocytes. CRD treatment elevated SLC7A11 and GPX4 expression in HG‐treated podocytes. The overexpression of SLC7A11 or GPX4 suppressed HG‐evoked apoptosis, inflammation, and ferroptosis in podocytes. Moreover, the silencing of SLC7A11 or GPX4 abolished the protective effects of CRD on HG‐treated podocytes. Moreover, CRD ameliorated renal structure injury and inflammation in STZ‐induced diabetic mice by modulating SLC7A11 or GPX4 expression. Conclusions Cordycepin suppressed HG‐induced apoptosis, inflammation, and ferroptosis in podocytes in vitro, and ameliorated renal injury and inflammation in STZ‐induced diabetic mice by activating the SLC7A11/GPX4 pathway.
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series Journal of Diabetes Investigation
spelling doaj-art-77b9944d37c94521b669cae9d1b54b112025-08-20T03:07:39ZengWileyJournal of Diabetes Investigation2040-11162040-11242025-06-01166992100010.1111/jdi.14407Cordycepin ameliorates diabetic nephropathy injury by activating the SLC7A11/GPX4 pathwayBing Wu0Jing Wang1Xiaohui Yan2Gang Jin3Qiong Wang4Department of Nephrology Shaanxi Provincial People's Hospital Xi'an Shaanxi ChinaDepartment of Nephrology Shaanxi Provincial People's Hospital Xi'an Shaanxi ChinaDepartment of Nephrology Shaanxi Provincial People's Hospital Xi'an Shaanxi ChinaDepartment of Nephrology Shaanxi Provincial People's Hospital Xi'an Shaanxi ChinaDepartment of Nephrology Shaanxi Provincial People's Hospital Xi'an Shaanxi ChinaABSTRACT Background Cordycepin (CRD) has been identified to alleviate diabetes‐induced injuries and complications including diabetic nephropathy (DN). Here, this work focused on probing the specific effects and potential mechanisms of CRD on DN progression. Methods High glucose (HG)‐induced mouse podocyte cell line (MPC5) was used for in vitro functional analyses. Cell proliferation and apoptosis were determined using cell counting kit‐8 assay, 5‐ethynyl‐2′‐deoxyuridine assay, and flow cytometry, respectively. ELISA analysis detected inflammatory factors. Cell ferroptosis was assessed by measuring the levels of Fe2+, glutathione, reactive oxygen species, and malonaldehyde. Results CRD treatment suppressed HG‐induced apoptosis, inflammation, and ferroptosis in podocytes. CRD treatment elevated SLC7A11 and GPX4 expression in HG‐treated podocytes. The overexpression of SLC7A11 or GPX4 suppressed HG‐evoked apoptosis, inflammation, and ferroptosis in podocytes. Moreover, the silencing of SLC7A11 or GPX4 abolished the protective effects of CRD on HG‐treated podocytes. Moreover, CRD ameliorated renal structure injury and inflammation in STZ‐induced diabetic mice by modulating SLC7A11 or GPX4 expression. Conclusions Cordycepin suppressed HG‐induced apoptosis, inflammation, and ferroptosis in podocytes in vitro, and ameliorated renal injury and inflammation in STZ‐induced diabetic mice by activating the SLC7A11/GPX4 pathway.https://doi.org/10.1111/jdi.14407CordycepinDiabetic nephropathyFerroptosis
spellingShingle Bing Wu
Jing Wang
Xiaohui Yan
Gang Jin
Qiong Wang
Cordycepin ameliorates diabetic nephropathy injury by activating the SLC7A11/GPX4 pathway
Journal of Diabetes Investigation
Cordycepin
Diabetic nephropathy
Ferroptosis
title Cordycepin ameliorates diabetic nephropathy injury by activating the SLC7A11/GPX4 pathway
title_full Cordycepin ameliorates diabetic nephropathy injury by activating the SLC7A11/GPX4 pathway
title_fullStr Cordycepin ameliorates diabetic nephropathy injury by activating the SLC7A11/GPX4 pathway
title_full_unstemmed Cordycepin ameliorates diabetic nephropathy injury by activating the SLC7A11/GPX4 pathway
title_short Cordycepin ameliorates diabetic nephropathy injury by activating the SLC7A11/GPX4 pathway
title_sort cordycepin ameliorates diabetic nephropathy injury by activating the slc7a11 gpx4 pathway
topic Cordycepin
Diabetic nephropathy
Ferroptosis
url https://doi.org/10.1111/jdi.14407
work_keys_str_mv AT bingwu cordycepinamelioratesdiabeticnephropathyinjurybyactivatingtheslc7a11gpx4pathway
AT jingwang cordycepinamelioratesdiabeticnephropathyinjurybyactivatingtheslc7a11gpx4pathway
AT xiaohuiyan cordycepinamelioratesdiabeticnephropathyinjurybyactivatingtheslc7a11gpx4pathway
AT gangjin cordycepinamelioratesdiabeticnephropathyinjurybyactivatingtheslc7a11gpx4pathway
AT qiongwang cordycepinamelioratesdiabeticnephropathyinjurybyactivatingtheslc7a11gpx4pathway