Polyunsaturated fatty acids ameliorate renal stone-induced renal tubular damage via miR-93-5p/Pknox1 axis

Liu, Qin; Tanida, Jun; Chen, Zhong; Wei, Lanji; Chen, Jianying; Xie, Zhigang

doi:10.1016/j.nut.2022.111863

Cited by 4 publications

(3 citation statements)

References 40 publications

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“…When miR-93-5p was downregulated or inhibited, polyunsaturated fatty acids (PUFA) reversed the effects of decreased apoptosis and fat accumulation in a mouse kidney stone model and COM-induced HK-2 cells. The overexpression of Pknox1 counteracted the effects of the miR-93-5p upregulation on HK-2 cells induced by COM, suggesting that PUFA can prevent tubular injury caused by renal stones by modulating the miR-93-5p/Pknox1 axis [64].…”

Section: Oxidative Stress and Renal Tubular Epithelial Cell (Rtec) In...mentioning

confidence: 92%

“…Liu et al found that the expression of miR-93-5p was significantly downregulated in urine and biopsy tissue samples from kidney stone patients, and the expression level of miR-93-5p was negatively correlated with Pknox1 [64]. When miR-93-5p was downregulated or inhibited, polyunsaturated fatty acids (PUFA) reversed the effects of decreased apoptosis and fat accumulation in a mouse kidney stone model and COM-induced HK-2 cells.…”

Section: Oxidative Stress and Renal Tubular Epithelial Cell (Rtec) In...mentioning

confidence: 99%

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Non-Coding RNAs in Kidney Stones

Wang,

Mi,

Bai

et al. 2024

Biomolecules

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Nephrolithiasis is a major public health concern associated with high morbidity and recurrence. Despite decades of research, the pathogenesis of nephrolithiasis remains incompletely understood, and effective prevention is lacking. An increasing body of evidence suggests that non-coding RNAs, especially microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), play a role in stone formation and stone-related kidney injury. MiRNAs have been studied quite extensively in nephrolithiasis, and a plethora of specific miRNAs have been implicated in the pathogenesis of nephrolithiasis, involving remarkable changes in calcium metabolism, oxalate metabolism, oxidative stress, cell–crystal adhesion, cellular autophagy, apoptosis, and macrophage (Mp) polarization and metabolism. Emerging evidence suggests a potential for miRNAs as novel diagnostic biomarkers of nephrolithiasis. LncRNAs act as competing endogenous RNAs (ceRNAs) to bind miRNAs, thereby modulating mRNA expression to participate in the regulation of physiological mechanisms in kidney stones. Small interfering RNAs (siRNAs) may provide a novel approach to kidney stone prevention and treatment by treating related metabolic conditions that cause kidney stones. Further investigation into these non-coding RNAs will generate novel insights into the mechanisms of renal stone formation and stone-related renal injury and might lead to new strategies for diagnosing and treating this disease.

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Section: Oxidative Stress and Renal Tubular Epithelial Cell (Rtec) In...mentioning

confidence: 92%

Section: Oxidative Stress and Renal Tubular Epithelial Cell (Rtec) In...mentioning

confidence: 99%

Non-Coding RNAs in Kidney Stones

Wang,

Mi,

Bai

et al. 2024

Biomolecules

View full text Add to dashboard Cite

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“…Polyunsaturated fatty acids (PUFAs) are the main targets of lipid peroxidation, and their incorporation into phospholipids, a key event in lipid hydroperoxide-induced ferroptosis, is dependent on acyl coenzyme A synthase long-chain family member 4 (ACSL4) ( 101 ). Instead of causing ferroptosis, PUFAs have been shown to reduce the COM-induced apoptosis of HK-2 cells and diminish kidney tubular damage in a renal-stone mouse model via the miR-93-5p/Pknox1 axis ( 102 ). Yes-associated protein can enhance ACSL4 expression, thereby inducing ferroptosis and increasing CaOx crystal-induced renal fibrosis ( 103 ).…”

Section: The Various Forms Of Cell Death and Urolithiasismentioning

confidence: 99%

Cell death‑related molecules and targets in the progression of urolithiasis (Review)

Wu,

Xue,

et al. 2024

Int J Mol Med

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Urolithiasis is a high-incidence disease caused by calcium oxalate (mainly), uric acid, calcium phosphate, struvite, apatite, cystine and other stones. The development of kidney stones is closely related to renal tubule cell damage and crystal adhesion and aggregation. Cell death, comprising the core steps of cell damage, can be classified into various types (i.e., apoptosis, ferroptosis, necroptosis and pyroptosis). Different crystal types, concentrations, morphologies and sizes cause tubular cell damage via the regulation of different forms of cell death. Oxidative stress caused by high oxalate or crystal concentrations is considered to be a precursor to a variety of types of cell death. In addition, complex crosstalk exists among numerous signaling pathways and their key molecules in various types of cell death. Urolithiasis is considered a metabolic disorder, and tricarboxylic acid cycle-related molecules, such as citrate and succinate, are closely related to cell death and the inhibition of stone development. However, a literature review of the associations between kidney stone development, metabolism and various types of cell death is currently lacking, at least to the best of our knowledge. Thus, the present review summarizes the major advances in the understanding of regulated cell death and urolithiasis progression.

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