ArticleOxidative medicine and cellular longevity2019
Inhibition of PRMT5 Attenuates Oxidative Stress-Induced Pyroptosis via Activation of the Nrf2/HO-1 Signal Pathway in a Mouse Model of Renal Ischemia-Reperfusion Injury.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed.
- PRMT5 Mediates Sepsis-Associated Lung Injury by Modulating JAK1 Arginine Methylation: A Mechanism Study.The Kaohsiung journal of medical sciences · 2026Article
- Review
- Camel Whey protein ameliorates type Ⅰ diabetic cardiomyopathy by mitigating oxidative stress, inflammation and apoptosis.Food science of animal resources · 2026Article
- Apoptosis, Pyroptosis, and Necroptosis (PANoptosis) may be Present in Renal Ischemic Injury.Current medicinal chemistry · 2026Article
- Quercetin Inhibits Ectopic Lesion Formation in Mice by Modulating the MAT2A/PRMT5 Pathway through PPARγ Activation.Combinatorial chemistry & high throughput screening · 2026Article
- Cross-talk among novel programmed cell death pathways: a decisive network in renal ischemia-reperfusion injury.Frontiers in immunology · 2026Review
- Protein arginine methyltransferases as regulators of cellular stress.Experimental neurology · 2025Review
- Dexmedetomidine plays a protective role in sepsis-associated myocardial injury by repressing PRMT5-mediated ferroptosis.Toxicology research · 2025Article
- RTA-408 attenuates the hepatic ischemia reperfusion injury in mice possibly by activating the Nrf2/HO-1 signaling pathway.Open life sciences · 2025Article
- Nanoparticles transfected with plasmid-encoded lncRNA-OIP5-AS1 inhibit renal ischemia-reperfusion injury in mice via the miR-410-3p/Nrf2 axis.Renal failure · 2024Article
- Protein Arginine Methyltransferases: Emerging Targets in Cardiovascular and Metabolic Disease.Diabetes & metabolism journal · 2024Review
- The emerging role of regulated cell death in ischemia and reperfusion-induced acute kidney injury: current evidence and future perspectives.Cell death discovery · 2024Review
- Article
- Diabetic Cardiomyopathy Uncovered: Transcriptomics, NLRP3, and Carvedilol Mechanisms.Journal of diabetes research · 2024Article
- Comprehensive molecular and cellular characterization of endoplasmic reticulum stress-related key genes in renal ischemia/reperfusion injury.Frontiers in immunology · 2024Article
- Artesunate-Nanoliposome-TPP, a Novel Drug Delivery System That Targets the Mitochondria, Attenuates Cisplatin-Induced Acute Kidney Injury by Suppressing Oxidative Stress and Inflammatory Effects.International journal of nanomedicine · 2024Article
- Attenuates reactive oxygen species: induced pyroptosis via activation of the Nrf2/HO-1 signal pathway in models of trigeminal neuralgia.Scientific reports · 2023Article
- Nephroprotective Effects of Cardamonin on Renal Ischemia Reperfusion Injury/UUO-Induced Renal Fibrosis.Journal of agricultural and food chemistry · 2023Article
- Inhibition of histone methyltransferase PRMT5 attenuates cisplatin-induced hearing loss through the PI3K/Akt-mediated mitochondrial apoptotic pathway.Journal of pharmaceutical analysis · 2023Article
- PRMT5 reduces immunotherapy efficacy in triple-negative breast cancer by methylating KEAP1 and inhibiting ferroptosis.Journal for immunotherapy of cancer · 2023Article
3 more citing papers are in PubMed but not listed here.
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Abstract
backgroundExtensive evidence has demonstrated that oxidative stress, pyroptosis, and proinflammatory programmed cell death are related to renal ischemia/reperfusion (I/R) injury. However, the underlying mechanism remains to be illustrated. Protein arginine methylation transferase 5 (PRMT5), which mediates arginine methylation involved in the regulation of epigenetics, exhibits a variety of biological functions and essential roles in diseases. The present study investigated the role of PRMT5 in oxidative stress and pyroptosis induced by I/R injury in a mouse model and in a hypoxia/reoxygenation (H/R) model of HK-2 cells.
methodsC57 mice were used as an animal model. All mice underwent right nephrectomy, and the left renal pedicles were either clamped or not. Renal I/R injury was induced by ligating the left renal pedicle for 30 min followed by reperfusion for 24 h. HK-2 cells were exposed to normal conditions or stimulation through H/R. EPZ015666(EPZ)-a selective potent chemical inhibitor-and small interfering RNA (siRNA) were administered to suppress the function and expression of PRMT5. The levels of urea nitrogen and creatinine in the serum and renal tissue injury were assessed. Immunohistochemistry, western blotting, and reverse transcription-polymerase chain reaction were used to evaluate pyroptosis-related proteins including nod-like receptor protein-3, ASC, caspase-1, caspase-11, GSDMD-N, and interleukin-1
resultsI/R or H/R induced an increase in the expression of PRMT5. Inhibition of PRMT5 by EPZ alleviated oxidative stress and I/R- or H/R-induced pyroptosis. In renal tissue, the application of EPZ promoted the proliferation of tubular epithelium. In addition, H/R-induced pyroptosis in HK-2 cells was dependent on oxidative stress in vitro. Administration of either EPZ or siRNA led to decreased expression of pyroptosis-related proteins. Inhibition of PRMT5 also attenuated the I/R- or H/R-induced oxidative stress in vivo and in HK-2 cells, respectively. It also resulted in a distinct decrease in the levels of malondialdehyde and H
conclusionPRMT5 is involved in ischemia- and hypoxia-induced oxidative stress and pyroptosis in vitro and in vivo. Inhibition of PRMT5 may ameliorate renal I/R injury by suppressing oxidative stress and pyroptosis via the activation of the Nrf2/HO-1 pathway, as well as promoting the proliferation of tubular epithelium. Therefore, PRMT5 may be a promising therapeutic target.
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