LncRNA PART1 alleviated myocardial ischemia/reperfusion injury via suppressing miR-503-5p/BIRC5 mediated mitochondrial apoptosis

Guo, Zhihao; Zhao, Ming; Jia, Guowei; Ma, Rui; Li, Meili

doi:10.1016/j.ijcard.2021.05.044

Cited by 21 publications

(15 citation statements)

References 28 publications

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“…In addition, some investigators found that USP22 and lncRNA PART1 expression was decreased in a MIR injury model. Rodents overexpressing USP22 or lncRNA PART1 were well resistant to I/R-induced oxidative stress and cardiac injury, which may be partly attributed to the elevated GSH content in the myocardium [ 251 , 252 ]. In particular, USP22 raised GSH content and reduced the occurrence of ferroptosis in cardiomyocytes by activating the Sirt1-p53/SLC7A11 axis [ 252 ].…”

Section: Increasing Gsh And/or Gsh-dependent Antioxidant Enzymes Dire...mentioning

confidence: 99%

“…Current gene therapy research aims to target, for example, upstream targets of the GSH system or molecules associated with it (such as Nrf2, GPX, SLC7A11), genes aberrantly expressed in myocardial injury, and noncoding RNAs regulating mRNA transcription [76,202,[250][251][252][253]. Recombinant human GPX4 alleviated ISO-induced myocardial ischemia injury [250].…”

Section: Increasing Gsh And/or Gsh-dependent Antioxidant Enzymes Dire...mentioning

confidence: 99%

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Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis

Tan

Yin

et al. 2023

Cell Death Dis

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The glutathione (GSH) system is considered to be one of the most powerful endogenous antioxidant systems in the cardiovascular system due to its key contribution to detoxifying xenobiotics and scavenging overreactive oxygen species (ROS). Numerous investigations have suggested that disruption of the GSH system is a critical element in the pathogenesis of myocardial injury. Meanwhile, a newly proposed type of cell death, ferroptosis, has been demonstrated to be closely related to the GSH system, which affects the process and outcome of myocardial injury. Moreover, in facing various pathological challenges, the mammalian heart, which possesses high levels of mitochondria and weak antioxidant capacity, is susceptible to oxidant production and oxidative damage. Therefore, targeted enhancement of the GSH system along with prevention of ferroptosis in the myocardium is a promising therapeutic strategy. In this review, we first systematically describe the physiological functions and anabolism of the GSH system, as well as its effects on cardiac injury. Then, we discuss the relationship between the GSH system and ferroptosis in myocardial injury. Moreover, a comprehensive summary of the activation strategies of the GSH system is presented, where we mainly identify several promising herbal monomers, which may provide valuable guidelines for the exploration of new therapeutic approaches.

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Section: Increasing Gsh And/or Gsh-dependent Antioxidant Enzymes Dire...mentioning

confidence: 99%

Section: Increasing Gsh And/or Gsh-dependent Antioxidant Enzymes Dire...mentioning

confidence: 99%

Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis

Tan

Yin

et al. 2023

Cell Death Dis

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“…A number of lncRNAs have been demonstrated to serve as competing endogenous (ce)RNAs of miRNAs in myocardial I/R injury progression. Guo et al ( 19 ) reported that lncRNA PART1 protects mitochondrial function via miR-503-5p/BIRC5 in myocardial I/R injury. A report from Li et al ( 20 ) noted that lncRNA XIST acts as a ceRNA of miR-133a to improve myocardial I/R injury by regulating of SOCS2 and inhibiting autophagy.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA SNHG16 attenuates myocardial ischemia‑reoxygenation injury via targeting miR‑183/FOXO1 axis

Geng

Xing

et al. 2023

Exp Ther Med

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Accumulating evidence shows that long non-coding RNAs (lncRNAs) are widely involved in cellular processes of myocardial ischemia/reperfusion (I/R). The present study investigated the functions of lncRNA SNHG16 in myocardial I/R and the mechanism mediated by SNHG16. The myocardial I/R rat and cell model and hypoxia/reoxygenation injury (H/R) models of H9C2 cardiomyocytes were established to detect the expression of SNHG16. Cell Counting Kit-8, flow cytometric and western blot assays were conducted to detect cell viability, apoptosis and protein expression. Myocardial cell apoptosis was assessed by TUNEL staining. Dual-luciferase gene reporter was applied to determine the interaction between the molecules. The expressions of SNHG16 were upregulated in myocardial I/R injury models. Inhibition of SNHG16 relieved myocardial I/R injury in vivo and in vitro silencing of SNHG16 alleviated H/R induced cardiomyocyte apoptosis. To explore the regulatory mechanism, it was discovered that SNHG16 directly interacted with miR-183, while forkhead box O1 (FoxO1) was a target of microRNA (miR)-183. Findings from rescue assays revealed that miR-183 inhibitor and upregulation of FOXO1 can rescue the effect of sh-SNHG16 on H/R-induced cardiomyocyte apoptosis. The results indicated that the lncRNA SNHG16/miR-183/FOXO1 axis exacerbated myocardial cell apoptosis in myocardial I/R injury, suggesting SNHG16 as a potential therapeutic target for myocardial I/R injury.

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“…Hirakawa et al [ 41 ] showed that overexpression of miR-503 in human endometriotic cyst stromal cells inhibited cell proliferation and induced cell apoptosis by downregulation of its targets cyclinD1, Bcl-2, Ras homology A (RhoA), Rho-associated coiled-coil-forming protein kinase (ROCK1), ROCK2, and vascular endothelial growth factor A. Min et al showed that miR-503 induced the apoptosis of dendritic cells in vivo and in vitro by directly targeting Bcl-2 [ 42 ]. Guo et al [ 43 ] reported that forced expression of miR-503 reduced the cell viability of neonatal mouse ventricle cells and induced cell apoptosis under H/R condition, while silencing of miR-503 recovered cell viability and alleviated cell apoptosis. Consistent with these studies, in our study, overexpression of miR-503 in H9c2 cells reduced cell viability under either normoxia or H/R condition and increased cell apoptosis under H/R condition, while inhibition of miR-503 reversed these effects under H/R condition.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-503 Exacerbates Myocardial Ischemia/Reperfusion Injury via Inhibiting PI3K/Akt- and STAT3-Dependent Prosurvival Signaling Pathways

Cai

Sun

et al. 2022

Oxidative Medicine and Cellular Longevity

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Acute myocardial infarction is a leading cause of death worldwide, while restoration of blood flow to previously ischemic myocardium may lead to ischemia/reperfusion (I/R) injury. Accumulated evidence shows that microRNAs play important roles in cardiovascular diseases. However, the potential role of microRNA-503 (miR-503) in myocardial I/R injury is little known. Thus, this study is aimed at determining whether and how miR-503 affects myocardial I/R injury in vivo and in vitro. A mouse model of myocardial I/R injury and H9c2 cell model of hypoxia/reoxygenation (H/R) injury were established. The postischemic cardiac miR-503 was downregulated in vivo and in vitro. Mechanistically, PI3K p85 and Bcl-2 are miR-503 targets. The post-ischemic cardiac PI3K p85 protein level was decreased in vivo. Agomir-503 treatment exacerbated H/R-induced injuries manifested as decreased cell viability, increased lactate dehydrogenase activity, and cell apoptosis. Agomir-503 treatment reduced cell viability under normoxia as well and reduced both PI3K p85 and Bcl-2 protein levels under either normoxia or H/R condition. It reduced phosphorylation of Stat3 (p-Stat3-Y705) and Akt (T450) in cells subjected to H/R. In contrast, Antagomir-503 treatment attenuated H/R injury and increased p-Stat3 (Y705) under normoxia and increased p-Akt (T450) under either normoxia or H/R condition. It is concluded that miR-503 exacerbated I/R injury via inactivation of PI3K/Akt and STAT3 pathways and may become a therapeutic target in preventing myocardial I/R injury.

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LncRNA PART1 alleviated myocardial ischemia/reperfusion injury via suppressing miR-503-5p/BIRC5 mediated mitochondrial apoptosis

Cited by 21 publications

References 28 publications

Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis

Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis

Knockdown of lncRNA SNHG16 attenuates myocardial ischemia‑reoxygenation injury via targeting miR‑183/FOXO1 axis

MicroRNA-503 Exacerbates Myocardial Ischemia/Reperfusion Injury via Inhibiting PI3K/Akt- and STAT3-Dependent Prosurvival Signaling Pathways

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