ArticleScientific reports2025
GOLPH3 promotes calcium oxalate-induced renal injury and fibrosis through Golgi stress-mediated apoptosis and inflammatory responses.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026Review
- KLF2 alleviates sepsis-induced acute kidney injury via the lncRNA GAS6-AS2/GOLPH3 axis.BMC nephrology · 2026Article
- Article
- Physiological roles of phosphoinositides and inositol phosphates: Implications for metabolic dysfunction-associated steatotic liver disease.Clinical science (London, England : 1979) · 2025Review
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7 authors.
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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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