GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses

Abstract A common urological disorder, calcium oxalate (CaOx) stones are the most common form of kidney stones. Deposition of CaOx crystals leads to tubular damage, interstitial fibrosis, and chronic kidney disease. Understanding the intrinsic mechanisms of kidney stone formation is essential for th...

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Main Authors: Bao-feng Song, Bo-jun Li, Yushi Sun, Ming Li, Ting Rao, Yuan Ruan, Fan Cheng
Format: Article
Language:English
Published: Nature Portfolio 2025-03-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-025-91638-0
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author Bao-feng Song
Bo-jun Li
Yushi Sun
Ming Li
Ting Rao
Yuan Ruan
Fan Cheng
author_facet Bao-feng Song
Bo-jun Li
Yushi Sun
Ming Li
Ting Rao
Yuan Ruan
Fan Cheng
author_sort Bao-feng Song
collection DOAJ
description Abstract A common urological disorder, calcium oxalate (CaOx) stones are the most common form of kidney stones. Deposition of CaOx crystals leads to tubular damage, interstitial fibrosis, and chronic kidney disease. Understanding the intrinsic mechanisms of kidney stone formation is essential for the prevention of kidney stones and the development of new therapeutic agents. The Golgi apparatus is a key organelle in the secretory pathway of eukaryotic cells, which plays an important role in the sorting, modification, and transport of proteins within the cell, and has been reported to be involved in several diseases, including prostate tumors, gastrointestinal tumors, sepsis, and so on. GOLPH3 is also known as GPP34, GMx33, or MIDAS. It is a glycoprotein that regulates traffic between the trans-Golgi network and the cell membrane. However, its role in renal injury caused by CaOx crystal deposition is still unclear. Results from immunohistochemistry, qRT-PCR, western blot, and public database single nucleotide RNA-seq showed that GOLPH3 was significantly upregulated in kidney stone patients and animal kidneys. Significant inhibition of Golgi stress, apoptosis, and renal fibrosis by GOLPH3 inhibition with siRNA in CaOx-stimulated HK-2 cells. The PI3K\AKT\mTOR signaling pathway was inhibited by GOLPH3 knockdown, which may be associated with reduced inflammatory response and apoptosis, as well as restoration of Golgi morphology and function. In conclusion, GOLPH3 plays a critical role in CaOx-induced kidney injury by promoting Golgi stress and increasing inflammatory responses, apoptosis, and renal fibrosis, suggesting that GOLPH3 is a potential therapeutic target for kidney stones.
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spelling doaj-art-1a5f9d00a72e40368126fa0b97bdfc1b2025-08-20T01:57:44ZengNature PortfolioScientific Reports2045-23222025-03-0115111310.1038/s41598-025-91638-0GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responsesBao-feng Song0Bo-jun Li1Yushi Sun2Ming Li3Ting Rao4Yuan Ruan5Fan Cheng6Department of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityDepartment of Urology, Renmin Hospital of Wuhan UniversityAbstract A common urological disorder, calcium oxalate (CaOx) stones are the most common form of kidney stones. Deposition of CaOx crystals leads to tubular damage, interstitial fibrosis, and chronic kidney disease. Understanding the intrinsic mechanisms of kidney stone formation is essential for the prevention of kidney stones and the development of new therapeutic agents. The Golgi apparatus is a key organelle in the secretory pathway of eukaryotic cells, which plays an important role in the sorting, modification, and transport of proteins within the cell, and has been reported to be involved in several diseases, including prostate tumors, gastrointestinal tumors, sepsis, and so on. GOLPH3 is also known as GPP34, GMx33, or MIDAS. It is a glycoprotein that regulates traffic between the trans-Golgi network and the cell membrane. However, its role in renal injury caused by CaOx crystal deposition is still unclear. Results from immunohistochemistry, qRT-PCR, western blot, and public database single nucleotide RNA-seq showed that GOLPH3 was significantly upregulated in kidney stone patients and animal kidneys. Significant inhibition of Golgi stress, apoptosis, and renal fibrosis by GOLPH3 inhibition with siRNA in CaOx-stimulated HK-2 cells. The PI3K\AKT\mTOR signaling pathway was inhibited by GOLPH3 knockdown, which may be associated with reduced inflammatory response and apoptosis, as well as restoration of Golgi morphology and function. In conclusion, GOLPH3 plays a critical role in CaOx-induced kidney injury by promoting Golgi stress and increasing inflammatory responses, apoptosis, and renal fibrosis, suggesting that GOLPH3 is a potential therapeutic target for kidney stones.https://doi.org/10.1038/s41598-025-91638-0Kidney stonesCaOxGOLPH3Golgi
spellingShingle Bao-feng Song
Bo-jun Li
Yushi Sun
Ming Li
Ting Rao
Yuan Ruan
Fan Cheng
GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses
Scientific Reports
Kidney stones
CaOx
GOLPH3
Golgi
title GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses
title_full GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses
title_fullStr GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses
title_full_unstemmed GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses
title_short GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses
title_sort golph3 promotes calcium oxalate induced renal injury and fibrosis through golgi stress mediated apoptosis and inflammatory responses
topic Kidney stones
CaOx
GOLPH3
Golgi
url https://doi.org/10.1038/s41598-025-91638-0
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