Suppression of lncRNA GAS6-AS2 alleviates sepsis-related acute kidney injury through regulating the miR-136-5p/OXSR1 axis <i>in vitro</i> and <i>in vivo</i>

Cui, Hongrui; Ren, Guangwei; Hu, Xiuhong; Xu, Bin; Li, Yuping; Niu, Zheli; Mu, Liqin

doi:10.1080/0886022x.2022.2092001

Cited by 4 publications

(2 citation statements)

References 52 publications

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“…Both long non-coding RNAs (lncRNAs) and microRNA (miRNA) have been suggested to play essential roles in various diseases, including SI-AKI (63,64). It is known that lncRNA regulates the activities of miRNA through the lncRNA-miRNA interactions.…”

Section: Non-coding Rnamentioning

confidence: 99%

Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection

et al. 2023

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Sepsis-induced acute kidney injury (SI-AKI), a common critically ill, represents one of the leading causes of global death. Emerging evidence reveals autophagy as a pivotal modulator of SI-AKI. Autophagy affects the cellular processes of renal lesions, including cell death, inflammation, and immune responses. Herein, we conducted a systematic and comprehensive review on the topic of the proposed roles of autophagy in SI-AKI. Forty-one relevant studies were finally included and further summarized and analyzed. This review revealed that a majority of included studies (24/41, 58.5%) showed an elevation of the autophagy level during SI-AKI, while 22% and 19.5% of the included studies reported an inhibition and an elevation at the early stage but a declination of renal autophagy in SI-AKI, respectively. Multiple intracellular signaling molecules and pathways targeting autophagy (e.g. mTOR, non-coding RNA, Sirtuins family, mitophagy, AMPK, ROS, NF-Kb, and Parkin) involved in the process of SI-AKI, exerting multiple biological effects on the kidney. Multiple treatment modalities (e.g. small molecule inhibitors, temsirolimus, rapamycin, polydatin, ascorbate, recombinant human erythropoietin, stem cells, Procyanidin B2, and dexmedetomidine) have been found to improve renal function, which may be attributed to the elevation of the autophagy level in SI-AKI. Though the exact roles of autophagy in SI-AKI have not been well elucidated, it may be implicated in preventing SI-AKI through various molecular pathways. Targeting the autophagy-associated proteins and pathways may hint towards a new prospective in the treatment of critically ill patients with SI-AKI, but more preclinical studies are still warranted to validate this hypothesis.

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Section: Non-coding Rnamentioning

confidence: 99%

Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection

et al. 2023

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“…In sepsis, lncRNAs regulate inflammation by acting as molecular scaffolds or decoys [ 19 , 20 ], influencing the expression of genes involved in inflammation [ 21 , 22 ], and modulating immune cell function and macrophage polarization [ 23 , 24 ]. LncRNAs can have both enhancing and suppressing effects on immune functions during sepsis [ 25 ], affecting the balance between pro-inflammatory and anti-inflammatory responses [ 26 , 27 , 28 ] and ultimately influencing the development of sepsis-associated organ dysfunction [ 22 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 ].…”

Section: Introductionmentioning

confidence: 99%

Circulating Exosomes from Septic Mice Activate NF-κB/MIR17HG Pathway in Macrophages

Wu,

Rau,

et al. 2024

Biomedicines

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Circulating exosomes derived from polymicrobial sepsis contain various non-coding RNAs and proteins. Isobaric tags for a relative or absolute quantitation proteomic analysis of the exosomal content revealed 70 dysregulated proteins in the circulating exosomes from septic mice. Next-generation sequencing was used to profile the long non-coding RNA expression in primary cultured macrophages treated with exosomes obtained from the blood of septic C57BL/6 mice, and it was discovered that the nuclear factor-kappa B (NF-κB)/miR-17-92a-1 cluster host gene (MIR17HG) pathways were activated in the macrophages. The inhibition of MIR17HG expression by RNA interference resulted in significantly decreased cell viability. RNA pull-down assays of MIR17HG revealed that ten protein targets bind to MIR17HG. Interaction networks of proteins pulled down by MIR17HG were constructed using GeneMANIA, and their functions were mainly involved in ribonucleoprotein granules, type I interferons, the regulation of organelle assembly, the biosynthesis of acetyl coenzyme A, as a signal transducer and activator of transcription (STAT) protein phosphorylation, and mRNA splicing. Furthermore, RNA interference inhibited MIR17HG expression, resulting in significantly decreased cell survival. In conclusion, this work discovered considerable MIR17HG overexpression in macrophages treated with circulating exosomes from sepsis-affected animals. This study’s findings assist us in comprehending the role of exosomes in modulating inflammatory responses and mediating pathogenic pathways in macrophages during sepsis.

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MiR-136-5p in cancer: Roles, mechanisms, and chemotherapy resistance

Zhang,

Xu,

Tong

et al. 2024

Gene

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Suppression of lncRNA GAS6-AS2 alleviates sepsis-related acute kidney injury through regulating the miR-136-5p/OXSR1 axis in vitro and in vivo

Cited by 4 publications

References 52 publications

Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection

Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection

Circulating Exosomes from Septic Mice Activate NF-κB/MIR17HG Pathway in Macrophages

MiR-136-5p in cancer: Roles, mechanisms, and chemotherapy resistance

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