MicroRNA-141-3p attenuates oxidative stress-induced hepatic ischemia reperfusion injury via Keap1/Nrf2 pathway

Li, Tingting; Chen, Qingsong; Dai, Jiangwen; Huang, Zuotian; Luo, Yunhai; Mou, Tong; Pu, Jing; Yang, Hang; Wei, Xufu; Wu, Zhongjun

doi:10.1007/s11033-022-07570-3

Cited by 7 publications

(3 citation statements)

References 31 publications

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“…32 Notably, miR-141-3p's antiapoptotic and anti-inflammatory effects extend to hepatocytes, where it attenuates ROS production and apoptosis during H/R insults. 13 Our study further corroborated these findings by demonstrating the DEX-induced upregulation of miR-141-3p, which may potentially inhibit inflammatory factors and apoptosis in cardiomyocytes, thereby warranting future investigation. Importantly, miR-141 has been implicated in the regulation of ferroptosis, iron metabolism, antioxidant metabolism, and lipid metabolism.…”

Section: Discussionsupporting

confidence: 80%

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DEX Inhibits H/R-induced Cardiomyocyte Ferroptosis by the miR-141-3p/lncRNA TUG1 Axis

Zhu,

Yuan,

Wen

et al. 2024

Thorac Cardiovasc Surg

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Background Ferroptosis is emerging as a critical pathway in ischemia/reperfusion (I/R) injury, contributing to compromised cardiac function and predisposing individuals to sepsis and myocardial failure. The study investigates the underlying mechanism of dexmedetomidine (DEX) in hypoxia/reoxygenation (H/R)-induced ferroptosis in cardiomyocytes, aiming to identify novel targets for myocardial I/R injury treatment. Methods H9C2 cells were subjected to H/R and treated with varying concentrations of DEX. Additionally, H9C2 cells were transfected with miR-141-3p inhibitor followed by H/R treatment. Levels of miR-141-3p, long noncoding RNA (lncRNA) taurine upregulated 1 (TUG1), Fe2+, glutathione (GSH), and malondialdehyde were assessed. Reactive oxygen species (ROS) generation was measured via fluorescent labeling. Expression of ferroptosis-related proteins glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long-chain family member 4 (ACSL4) was determined using Western blot. The interaction between miR-141-3p and lncRNA TUG1 was evaluated through RNA pull-down assay and dual-luciferase reporter gene assays. The stability of lncRNA TUG1 was assessed using actinomycin D. Results DEX ameliorated H/R-induced cardiomyocyte injury and elevated miR-141-3p expression in cardiomyocytes. DEX treatment increased cell viability, Fe2+, and ROS levels while decreasing ACSL4 protein expression. Furthermore, DEX upregulated GSH and GPX4 protein levels. miR-141-3p targeted lncRNA TUG1, reducing its stability and overall expression. Inhibition of miR-141-3p or overexpression of lncRNA TUG1 partially reversed the inhibitory effect of DEX on H/R-induced ferroptosis in cardiomyocytes. Conclusion DEX mitigated H/R-induced ferroptosis in cardiomyocytes by upregulating miR-141-3p expression and downregulating lncRNA TUG1 expression, unveiling a potential therapeutic strategy for myocardial I/R injury.

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Section: Discussionsupporting

confidence: 80%

“…12 Previous investigations have shown that miR-141-3p is downregulated in cardiomyocytes subjected to hypoxia/reoxygenation (H/R), and its overexpression attenuates cell apoptosis and oxidative stress under H/R conditions. 13,14 However, the mechanistic link between miR-141-3p and I/R injury via ferroptosis remains unexplored.…”

Section: Introductionmentioning

confidence: 99%

DEX Inhibits H/R-induced Cardiomyocyte Ferroptosis by the miR-141-3p/lncRNA TUG1 Axis

Zhu,

Yuan,

Wen

et al. 2024

Thorac Cardiovasc Surg

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“…Of note, several miRNAs have been indicated to participate in the hepatoprotective effect of several pharmacological agents during HIRI, including inhaled anesthetics and propofol. For instance, sevoflurane preconditioning ameliorates liver injury by the inhibitory effects of several miRNAs ( e.g ., miR-133 and miR-205) on the Akt–GSK–cyclin D1 pathway[ 89 ]. Others have reported that sevoflurane preconditioning promotes the expression of miR-96 and inhibits FOXO4, thus alleviating HIRI[ 90 ].…”

Section: Mirnasmentioning

confidence: 99%

Non-coding RNAs: The potential biomarker or therapeutic target in hepatic ischemia-reperfusion injury

Shao,

Wang,

Xiao

et al. 2023

World J Gastroenterol

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Delayed passage of meconium or constipation during the perinatal period is traditionally regarded as a signal to initiate further work up to evaluate for serious diagnoses such as Hirschsprung’s disease (HD), meconium ileus due to Cystic Fibrosis, etc. The diagnosis of HD particularly warrants invasive testing to confirm the diagnosis, such as anorectal manometry or rectal suction biopsy. What if there was another etiology of perinatal constipation, that is far lesser known? Cow’s milk protein allergy (CMPA) is often diagnosed in infants within the first few weeks of life, however, there are studies that show that the CMPA allergen can be passed from mother to an infant in-utero, therefore allowing symptoms to show as early as day one of life. The presentation is more atypical, with perinatal constipation rather than with bloody stools, diarrhea, and vomiting. The diagnosis and management would be avoidance of cow's milk protein within the diet, with results and symptom improvement in patients immediately. Therefore, we discuss whether an alternative pathway to address perinatal constipation should be further discussed and implemented to potentially avoid invasive techniques in patients. This entails first ruling out CMPA with safe, noninvasive techniques with diet modification, and if unsuccessful, then moving forward with further diagnostic modalities.

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miR-141-3p attenuates inflammation and oxidative stress–induced pulmonary fibrosis in ARDS via the Keap1/Nrf2/ARE signaling pathway

Long,

Zhang,

Yang

et al. 2024

Immunol Res

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MicroRNA-141-3p attenuates oxidative stress-induced hepatic ischemia reperfusion injury via Keap1/Nrf2 pathway

Cited by 7 publications

References 31 publications

DEX Inhibits H/R-induced Cardiomyocyte Ferroptosis by the miR-141-3p/lncRNA TUG1 Axis

DEX Inhibits H/R-induced Cardiomyocyte Ferroptosis by the miR-141-3p/lncRNA TUG1 Axis

Non-coding RNAs: The potential biomarker or therapeutic target in hepatic ischemia-reperfusion injury

miR-141-3p attenuates inflammation and oxidative stress–induced pulmonary fibrosis in ARDS via the Keap1/Nrf2/ARE signaling pathway

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