Advances in the study of RNA-binding proteins in diabetic complications

Chen, Xinyue; Wu, Jiasheng; Li, Zhangwang; Han, Jiashu; Xia, Panpan; Shen, Yue; Ma, Jianyong; Zhang, Jing; Yu, Peng

doi:10.1016/j.molmet.2022.101515

Cited by 9 publications

(5 citation statements)

References 198 publications

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“…Furthermore, our findings specify that the mRNA translation mediated by RBPs, particularly IGF2BPs, contributes to the development of HFD-induced T2D. Recent studies have highlighted the significant roles of mitochondrial translation and RBPs in the development of insulin resistance and T2D [35][36][37][38]. Our data provide valuable insights into the interplay between these mechanisms, underscoring their interconnectedness.…”

Section: Discussionsupporting

confidence: 65%

D-Allulose Ameliorates Dysregulated Macrophage Function and Mitochondrial NADH Homeostasis, Mitigating Obesity-Induced Insulin Resistance

Bae,

Shin,

Han

et al. 2023

Nutrients

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D-allulose, a rare sugar, has been proposed to have potential benefits in addressing metabolic disorders such as obesity and type 2 diabetes (T2D). However, the precise mechanisms underlying these effects remain poorly understood. We aimed to elucidate the mechanisms by which D-allulose influences obesity-induced insulin resistance. We conducted gene set enrichment analysis on the liver and white adipose tissue of mice exposed to a high-fat diet (HFD) along with the white adipose tissue of individuals with obesity. Our study revealed that D-allulose effectively suppressed IFN-γ, restored chemokine signaling, and enhanced macrophage function in the livers of HFD-fed mice. This implies that D-allulose curtails liver inflammation, alleviating insulin resistance and subsequently impacting adipose tissue. Furthermore, D-allulose supplementation improved mitochondrial NADH homeostasis and translation in both the liver and white adipose tissue of HFD-fed mice. Notably, we observed decreased NADH homeostasis and mitochondrial translation in the omental tissue of insulin-resistant obese subjects compared to their insulin-sensitive counterparts. Taken together, these results suggest that supplementation with allulose improves obesity-induced insulin resistance by mitigating the disruptions in macrophage and mitochondrial function. Furthermore, our data reinforce the crucial role that mitochondrial energy expenditure plays in the development of insulin resistance triggered by obesity.

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Section: Discussionsupporting

confidence: 65%

D-Allulose Ameliorates Dysregulated Macrophage Function and Mitochondrial NADH Homeostasis, Mitigating Obesity-Induced Insulin Resistance

Bae,

Shin,

Han

et al. 2023

Nutrients

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“…HuR has the ability to modulate inflammatory responses in renal injury (Chen et al, 2022b), muscular dystrophy (Mubaid et al, 2019), and intervertebral disc degeneration (Shao et al, 2020). The increased secretion of inflammatory cytokines in the acute phase of SCI plays an important role in tissue damage.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Relieves HuR/KLF9-Mediated Inflammation to Enhance Neurological Repair after Spinal Cord Injury

Zhang,

Xu,

et al. 2023

eNeuro

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Electroacupuncture (EA) is widely applied in clinical therapy for spinal cord injury (SCI). However, the associated molecular mechanism has yet to be elucidated. The current study aimed to investigate the underlying mechanism of EA in neurologic repair after SCI. First, we investigated the role of EA in the neurologic repair of the SCI rat model. The expression levels of human antigen R (HuR) and Krüppel-like factor 9 (KLF9) in spinal cord tissues were quantified after treatment. Second, we conducted bioinformatics analysis, RNA pull-down assays, RNA immunoprecipitation, and luciferase reporter gene assay to verify the binding of HuR and KLF9 mRNA for mRNA stability. Last, HuR inhibitor CMLD-2 was used to verify the enhanced effect of EA on neurologic repair after SCI via the HuR/KLF9 axis. Our data provided convincing evidence that EA facilitated the recovery of neuronal function in SCI rats by reducing apoptosis and inflammation of neurons. We found that EA significantly diminished the SCI-mediated upregulation of HuR, and HuR could bind to the 3′ untranslated region of KLF9 mRNA to protect its decay. In addition, a series ofin vivoexperiments confirmed that CMLD-2 administration increased EA-mediated pain thresholds and motor function in SCI rats. Collectively, the present study showed that EA improved pain thresholds and motor function in SCI rats via impairment of HuR-mediated KLF9 mRNA stabilization, thus providing a better understanding of the regulatory mechanisms regarding EA-mediated neurologic repair after SCI.

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“…This part has been well-reviewed. [422][423][424][425] Recently, Marcheva et al 426 reported that AS participates in the regulation of circadian rhythm in pancreatic β cells. thyroid hormone receptor-associated protein 3 (THRAP3) regulates circadian rhythm-dependent ASE by binding to exons flanking the coding sequence that is more often skipped in clock mutant β cells.…”

Section: Colorectal Cancer (Crc)mentioning

confidence: 99%

Alternative splicing and related RNA binding proteins in human health and disease

Tao,

Zhang,

Wang

et al. 2024

Sig Transduct Target Ther

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Alternative splicing (AS) serves as a pivotal mechanism in transcriptional regulation, engendering transcript diversity, and modifications in protein structure and functionality. Across varying tissues, developmental stages, or under specific conditions, AS gives rise to distinct splice isoforms. This implies that these isoforms possess unique temporal and spatial roles, thereby associating AS with standard biological activities and diseases. Among these, AS-related RNA-binding proteins (RBPs) play an instrumental role in regulating alternative splicing events. Under physiological conditions, the diversity of proteins mediated by AS influences the structure, function, interaction, and localization of proteins, thereby participating in the differentiation and development of an array of tissues and organs. Under pathological conditions, alterations in AS are linked with various diseases, particularly cancer. These changes can lead to modifications in gene splicing patterns, culminating in changes or loss of protein functionality. For instance, in cancer, abnormalities in AS and RBPs may result in aberrant expression of cancer-associated genes, thereby promoting the onset and progression of tumors. AS and RBPs are also associated with numerous neurodegenerative diseases and autoimmune diseases. Consequently, the study of AS across different tissues holds significant value. This review provides a detailed account of the recent advancements in the study of alternative splicing and AS-related RNA-binding proteins in tissue development and diseases, which aids in deepening the understanding of gene expression complexity and offers new insights and methodologies for precision medicine.

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Advances in the study of RNA-binding proteins in diabetic complications

Cited by 9 publications

References 198 publications

D-Allulose Ameliorates Dysregulated Macrophage Function and Mitochondrial NADH Homeostasis, Mitigating Obesity-Induced Insulin Resistance

D-Allulose Ameliorates Dysregulated Macrophage Function and Mitochondrial NADH Homeostasis, Mitigating Obesity-Induced Insulin Resistance

Electroacupuncture Relieves HuR/KLF9-Mediated Inflammation to Enhance Neurological Repair after Spinal Cord Injury

Alternative splicing and related RNA binding proteins in human health and disease

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