ArticleOxidative medicine and cellular longevity2021
The Suppression of Pin1-Alleviated Oxidative Stress through the p38 MAPK Pathway in Ischemia- and Reperfusion-Induced Acute Kidney Injury.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- The novel circular RNA circG6pc attenuates oxidative stress and mitochondrial damage through miR-7018-5p/Aldh6a1 axis in kidney fibrosis.Cellular & molecular biology letters · 2025Article
- Long Noncoding RNA SNHG12 Regulates Ischemia/reperfusion (I/R)-mediated Acute Kidney Injury (AKI) Through miR-129-1-3p/Ubiquitin Specific Peptidase 25 axis.Applied biochemistry and biotechnology · 2025Article
- Function and Mechanism of Abscisic Acid on Microglia-Induced Neuroinflammation in Parkinson's Disease.International journal of molecular sciences · 2024Review
- The molecular mechanisms of peptidyl-prolylFrontiers in pharmacology · 2024Review
- Sufentanil inhibits Pin1 to attenuate renal tubular epithelial cell ischemia-reperfusion injury by activating the PI3K/AKT/FOXO1 pathway.International urology and nephrology · 2023Article
- Estradiol regulates oxidative stress and angiogenesis of myocardial microvascular endothelial cells via the CDK1/CDK2 pathway.Heliyon · 2023Article
- Puerarin alleviated oxidative stress and ferroptosis during renal fibrosis induced by ischemia/reperfusion injury via TLR4/Nox4 pathway in rats.Acta cirurgica brasileira · 2023Article
- Circular RNA_HIPK3-Targeting miR-93-5p Regulates KLF9 Expression Level to Control Acute Kidney Injury.Computational and mathematical methods in medicine · 2023Article
- PIN1-mediated ROS production is involved in antagonism of N-acetyl-L-cysteine against arsenic-induced hepatotoxicity.Toxicology research · 2022Article
- Protective effects of mefunidone on ischemia-reperfusion injury/Folic acid-induced acute kidney injury.Frontiers in pharmacology · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPin1, as the peptidyl-prolyl isomerase, plays a vital role in cellular processes. However, whether it has a regulatory effect on renal ischemia and reperfusion (I/R) injury still remains unknown.
methodsThe hypoxia/reoxygenation (H/R) model in human kidney (HK-2) cells and the I/R model in rats were assessed to investigate the role of Pin1 on I/R-induced acute kidney injury. Male Sprague-Dawley rats were used to establish the I/R model for 15, 30, and 45 min ischemia and then 24 h reperfusion, with or without the Pin1 inhibitor, to demonstrate the role of Pin1 in acute kidney injury. HK-2 cells were cultured and experienced the H/R model to identify the molecular mechanisms involved.
resultsIn this study, we found that Pin1 and oxidative stress were obviously increased after renal I/R. Inhibition of Pin1 with juglone decreased renal structural and functional injuries, as well as oxidative stress. Besides, Pin1 inhibition with the inhibitor, juglone, or the small interfering RNA showed significant reduction on oxidative stress markers caused by the H/R process in vitro. Furthermore, the results indicated that the expression of p38 MAPK was increased during H/R in vitro and Pin1 inhibition could reduce the increased expression of p38 MAPK.
conclusionOur results illustrated that Pin1 aggravated renal I/R injury via elevating oxidative stress through activation of the p38 MAPK pathway. These findings indicated that Pin1 might become the potential treatment for renal I/R injury.
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