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PPARγ agonist alleviates calcium oxalate nephrolithiasis by regulating mitochondrial dynamics in renal tubular
Junfa Liu1, Xingyang Liu2, Lizhe Guo2
1Department of Urology, The Second Xiangya Hospital, Central South University, Changsha, China.
Background:
Kidney stone formation is a common disease that causes a significant threat to human health. The crystallization mechanism of calcium oxalate, the most common type of kidney stone, has been extensively researched, yet the damaging effects and mechanisms of calcium oxalate crystals on renal tubular epithelial cells remain incompletely elucidated. Regulated mitochondrial dynamics is essential for eukaryotic cells, but its role in the occurrence and progression of calcium oxalate (CaOx) nephrolithiasis is not yet understood.
Methods:
An animal model of calcium oxalate-related nephrolithiasis was established in adult male Sprague‒Dawley (SD) rats by continuously administering drinking water containing 1% ethylene glycol for 28 days. The impact of calcium oxalate crystals on mitochondrial dynamics and apoptosis in renal tubular epithelial cells was investigated using HK2 cells in vitro. Blood samples and bilateral kidney tissues were collected for histopathological evaluation and processed for tissue injury, inflammation, fibrosis, oxidative stress detection, and mitochondrial dynamics parameter analysis.
Results:
Calcium oxalate crystals caused higher levels of mitochondrial fission and apoptosis in renal tubular epithelial cells both in vivo and in vitro. Administration of a PPARγ agonist significantly alleviated mitochondrial fission and apoptosis in renal tubular epithelial cells, and improved renal function, accompanied by reduced levels of oxidative stress, increased antioxidant enzyme expression, alleviation of inflammation, and reduced fibrosis in vivo.
Conclusion:
Our results indicated that increased mitochondrial fission in renal tubular epithelial cells is a critical component of kidney injury caused by calcium oxalate stones, leading to the accumulation of reactive oxygen species within the tissue and the subsequent initiation of apoptosis. Regulating mitochondrial dynamics represents a promising approach for calcium oxalate nephrolithiasis.
Insights
Calcium oxalate crystals damage kidney cells by increasing mitochondrial fission and apoptosis. Targeting mitochondrial dynamics offers a promising therapeutic strategy for kidney stones.
Area of Science:
- Nephrology
- Cell Biology
- Biochemistry
Background:
- Kidney stones, particularly calcium oxalate stones, pose a significant health risk.
- The precise mechanisms by which calcium oxalate crystals damage renal tubular epithelial cells are not fully understood.
- The role of mitochondrial dynamics in calcium oxalate nephrolithiasis remains unclear.
Purpose of the Study:
- To investigate the effects of calcium oxalate crystals on mitochondrial dynamics and apoptosis in renal tubular epithelial cells.
- To explore the potential of regulating mitochondrial dynamics as a therapeutic strategy for calcium oxalate nephrolithiasis.
Main Methods:
- An in vivo rat model of calcium oxalate nephrolithiasis was established using ethylene glycol administration.
- In vitro studies utilized HK2 cells exposed to calcium oxalate crystals.
- Kidney tissues and blood samples were analyzed for histopathology, oxidative stress, inflammation, fibrosis, and mitochondrial dynamics.
Main Results:
- Calcium oxalate crystals induced significant mitochondrial fission and apoptosis in renal tubular epithelial cells.
- Treatment with a PPARγ agonist ameliorated mitochondrial fission and apoptosis, improved renal function, and reduced oxidative stress, inflammation, and fibrosis.
- Increased mitochondrial fission was linked to reactive oxygen species accumulation and apoptosis initiation.
Conclusions:
- Mitochondrial fission is a key factor in kidney injury induced by calcium oxalate stones.
- Regulating mitochondrial dynamics presents a potential therapeutic avenue for treating calcium oxalate nephrolithiasis.
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