Circulating small extracellular vesicle-encapsulated SEMA5A-IT1 attenuates myocardial ischemia–reperfusion injury after cardiac surgery with cardiopulmonary bypass

Wu, Ting; Shi, Guoning; Ji, Zhenhua; Wang, Shu; Geng, Lizhu; Guo, Zhigang

doi:10.1186/s11658-022-00395-9

Cited by 20 publications

(8 citation statements)

References 41 publications

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“…Extracellular vesicles (EVs) originate from endosomes, with diameters ranging between 30 and 150 nm; they are frequently detected in urine, blood, and cerebrospinal fluid [ 5 ]. EVs carry cargo containing multiple cellular components (DNA, lipids, proteins), transposable elements, and RNA (coding and noncoding) [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Extracellular vesicles derived from CD4+ T cells carry DGKK to promote sepsis-induced lung injury by regulating oxidative stress and inflammation

Zhang

et al. 2023

Cell Mol Biol Lett

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Background Sepsis is an abnormal immune response after infection, wherein the lung is the most susceptible organ to fail, leading to acute lung injury. To overcome the limitations of current therapeutic strategies and develop more specific treatment, the inflammatory process, in which T cell-derived extracellular vesicles (EVs) play a central role, should be explored deeply. Methods Liquid chromatography–tandem mass spectrometry was performed for serum EV protein profiling. The serum diacylglycerol kinase kappa (DGKK) and endotoxin contents of patients with sepsis-induced lung injury were measured. Apoptosis, oxidative stress, and inflammation in A549 cells, bronchoalveolar lavage fluid, and lung tissues of mice were measured by flow cytometry, biochemical analysis, enzyme-linked immunosorbent assay, quantitative real-time polymerase chain reaction, and western blot. Results DGKK, the key regulator of the diacylglycerol (DAG)/protein kinase C (PKC) pathway, exhibited elevated expression in serum EVs of patients with sepsis-induced lung injury and showed strong correlation with sepsis severity and disease progression. DGKK was expressed in CD4+ T cells under regulation of the NF-κB pathway and delivered by EVs to target cells, including alveolar epithelial cells. EVs produced by CD4+ T lymphocytes exerted toxic effects on A549 cells to induce apoptotic cell death, oxidative cell damage, and inflammation. In mice with sepsis induced by cecal ligation and puncture, EVs derived from CD4+ T cells also promoted tissue damage, oxidative stress, and inflammation in the lungs. These toxic effects of T cell-derived EVs were attenuated by the inhibition of PKC and NOX4, the downstream effectors of DGKK and DAG. Conclusions This approach established the mechanism that T-cell-derived EVs carrying DGKK triggered alveolar epithelial cell apoptosis, oxidative stress, inflammation, and tissue damage in sepsis-induced lung injury through the DAG/PKC/NOX4 pathway. Thus, T-cell-derived EVs and the elevated distribution of DGKK should be further investigated to develop therapeutic strategies for sepsis-induced lung injury.

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Section: Introductionmentioning

confidence: 99%

Extracellular vesicles derived from CD4+ T cells carry DGKK to promote sepsis-induced lung injury by regulating oxidative stress and inflammation

Zhang

et al. 2023

Cell Mol Biol Lett

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“… 396 Upregulation of LncRNA SEMA5A-IT1 protects cardiomyocytes against hypoxia/reoxygenation (H/R) injury partially through inhibition of ferroptosis by sponging miR-143-3p to upregulate SLC7A11. 397 miR-210-3p attenuates myocardial cell injury induced by H/R through inhibition of ferroptosis by downregulating TfR1. 398 miR-190a-5p promotes ferroptosis through inhibition of GLS2 expression.…”

Section: Epigenetic and Posttranslational Modifications Regulating Fe...mentioning

confidence: 99%

“… 396 MIRI ncRNA SLC7A11 Upregulated LncRNA SEMA5A-IT1 inhibits cardiomyocytes against hypoxia/reoxygenation injury partly through inhibiting ferroptosis via upregulating SLC7A11 by sponging miR-143-3p. 397 MIRI ncRNA TfR1 miR-210-3p alleviate hypoxia/reoxygenation-induced myocardial cell injury through inhibiting ferroptosis via dowregulating TfR1. 398 MIRI ncRNA GLS2 miR-190a-5p promotes ferroptosis through inhibiting GLS2.…”

Section: Epigenetic and Posttranslational Modifications Regulating Fe...mentioning

confidence: 99%

Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases

Wang,

Hu,

et al. 2023

Sig Transduct Target Ther

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Ferroptosis, a unique modality of cell death with mechanistic and morphological differences from other cell death modes, plays a pivotal role in regulating tumorigenesis and offers a new opportunity for modulating anticancer drug resistance. Aberrant epigenetic modifications and posttranslational modifications (PTMs) promote anticancer drug resistance, cancer progression, and metastasis. Accumulating studies indicate that epigenetic modifications can transcriptionally and translationally determine cancer cell vulnerability to ferroptosis and that ferroptosis functions as a driver in nervous system diseases (NSDs), cardiovascular diseases (CVDs), liver diseases, lung diseases, and kidney diseases. In this review, we first summarize the core molecular mechanisms of ferroptosis. Then, the roles of epigenetic processes, including histone PTMs, DNA methylation, and noncoding RNA regulation and PTMs, such as phosphorylation, ubiquitination, SUMOylation, acetylation, methylation, and ADP-ribosylation, are concisely discussed. The roles of epigenetic modifications and PTMs in ferroptosis regulation in the genesis of diseases, including cancers, NSD, CVDs, liver diseases, lung diseases, and kidney diseases, as well as the application of epigenetic and PTM modulators in the therapy of these diseases, are then discussed in detail. Elucidating the mechanisms of ferroptosis regulation mediated by epigenetic modifications and PTMs in cancer and other diseases will facilitate the development of promising combination therapeutic regimens containing epigenetic or PTM-targeting agents and ferroptosis inducers that can be used to overcome chemotherapeutic resistance in cancer and could be used to prevent other diseases. In addition, these mechanisms highlight potential therapeutic approaches to overcome chemoresistance in cancer or halt the genesis of other diseases.

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“…Transported to cardiomyocytes via sEVs, SEMA5A-IT1 acts as a cytoplasmic miRNA sponge, specifically interacting with miR-143-3p, preventing it from binding to target mRNAs, including BCL2 and SLC7A11. Elevated SEMA5A-IT1 levels protect cardiomyocytes against hypoxia/reoxygenation (H/R) injury, evidenced by increased viability, reduced apoptosis, and inhibition of ferroptosis ( Figure 3 ) ( Wu et al, 2022a ).…”

Section: Exosomal Ferroptosis-related Ncrnas In Pathogenesis Of Human...mentioning

confidence: 99%

Ferroptosis-related exosomal non-coding RNAs: promising targets in pathogenesis and treatment of non-malignant diseases

Zhang,

Xie

2024

Front. Cell Dev. Biol.

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Ferroptosis, an iron-dependent form of programmed cell death, introduces a novel perspective on cellular demise. This study investigates the regulatory network of exosomal non-coding RNAs (ncRNAs), including miRNAs, circRNAs, and lncRNAs, in ferroptosis modulation. The primary goal is to examine the pathological roles of ferroptosis-related exosomal ncRNAs, particularly in ischemic reperfusion injuries. The research reveals intricate molecular interactions governing the regulatory interplay between exosomal ncRNAs and ferroptosis, elucidating their diverse roles in different non-malignant pathological contexts. Attention is given to their impact on diseases, including cardiac, cerebral, liver, and kidney ischemic injuries, as well as lung, wound, and neuronal injuries. Beyond theoretical exploration, the study provides insights into potential therapeutic applications, emphasizing the significance of mesenchymal stem cells (MSCs)-derived exosomes. Findings underscore the pivotal role of MSC-derived exosomal ncRNAs in modulating cellular responses related to ferroptosis regulation, introducing a cutting-edge dimension. This recognition emphasizes the importance of MSC-derived exosomes as crucial mediators with broad therapeutic implications. Insights unveil promising avenues for targeted interventions, capitalizing on the diverse roles of exosomal ncRNAs, providing a comprehensive foundation for future therapeutic strategies.

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Circulating small extracellular vesicle-encapsulated SEMA5A-IT1 attenuates myocardial ischemia–reperfusion injury after cardiac surgery with cardiopulmonary bypass

Cited by 20 publications

References 41 publications

Extracellular vesicles derived from CD4+ T cells carry DGKK to promote sepsis-induced lung injury by regulating oxidative stress and inflammation

Extracellular vesicles derived from CD4+ T cells carry DGKK to promote sepsis-induced lung injury by regulating oxidative stress and inflammation

Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases

Ferroptosis-related exosomal non-coding RNAs: promising targets in pathogenesis and treatment of non-malignant diseases

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