Promising diagnostic and therapeutic circRNAs for skeletal and chondral disorders

Chen, Gaoyang; Tang, Wanze; Wang, Shang; Long, Canling; He, Xiaoqin; Yang, Dazhi; Peng, Songlin

doi:10.7150/ijbs.57887

Cited by 17 publications

(8 citation statements)

References 125 publications

(60 reference statements)

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“…Insufficient bone formation ability can lead to increased bone loss, thereby accelerating the progression of osteoporosis 1 . Many studies have confirmed that circRNAs play a critical role in the osteogenic differentiation of BMSCs 17,29 . Yin and Xue 30 found that hsa_circ_0006859 could promote the progression of osteoporosis by inhibiting miR‐642b‐5p/miR‐483‐3p and increasing the expression of EFNA2/DOCK3.…”

Section: Discussionmentioning

confidence: 99%

“…In recent years, circular RNAs (circRNAs) have been considered key regulators for posttranscriptional level regulation due to their stable circular structure 15 . Recent studies have suggested that circRNAs play key regulatory roles in the osteogenic differentiation process of BMSCs 16,17 . However, the current lack of targeted vectors limits the translational application of circRNA in the treatment of PMOP.…”

Section: Introductionmentioning

confidence: 99%

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Exosomal circFAM63Bsuppresses bone regeneration of postmenopausal osteoporosis via regulating miR‐578/HMGA2 axis

Li,

Zhao,

Zhang

et al. 2024

Journal Orthopaedic Research

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Postmenopausal osteoporosis (PMOP) affects hundreds of millions of elderly women worldwide. The imbalance between osteoblast‐mediated bone formation and osteoclast‐mediated bone resorption is the key factor in the progression of PMOP. Recently, exosomal circRNAs have been considered as critical regulators in physiological and pathological progress. However, their roles in PMOP still require further exploration. Herein, we identified that the expression ofexosomalcircFAM63B significantly increased in PMOP patients and is closely related to bone density. We further demonstrated that circFAM63B inhibits osteogenic differentiation of BMSCs and bone formation in OVX mice by using a combination of in vitro and in vivoexperiment strategies. Mechanistically, circFAM63B promotes HMGA2 expression by inhibiting miR‐578, thereby suppressing bone repair. Our study proved that exosomal circFAM63B suppresses the bone regeneration of postmenopausal osteoporosis by regulating the miR‐578/HMGA2 axis, which may provide new insights into the pathogenesis and development of PMOP. Knocking down exosomal circFAM63Bcould be regarded as a new strategy for the treatment of PMOP.This article is protected by copyright. All rights reserved.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Exosomal circFAM63Bsuppresses bone regeneration of postmenopausal osteoporosis via regulating miR‐578/HMGA2 axis

Li,

Zhao,

Zhang

et al. 2024

Journal Orthopaedic Research

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“…24,33 MiRNAs, assisted by ago protein, can recognize the 3'UTR end of the mRNA and induce its degradation. 34,35 Studies have shown that many miRNAs are differentially expressed in OA articular cartilage and play key regulatory roles. 36,37 However, the expression profiles of miRNAs in DDH-OA have not yet been reported.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐34a‐5p promotes the progression of osteoarthritis secondary to developmental dysplasia of the hip by restraining SESN2‐induced autophagy

Wang

Guo

et al. 2023

Journal Orthopaedic Research

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Osteoarthritis (OA), a late‐stage complication of developmental dysplasia of the hip (DDH), is a key factor leading to further degeneration of joint function. Studies have shown that Sestrin2 (SESN2) is a positive regulator in protecting articular cartilage from degradation. However, the regulatory effects of SESN2 on DDH‐OA and its upstream regulators remain obscure. Here, we first identified that the expression of SESN2 significantly decreased in the cartilage of DDH‐OA samples, with an expression trend negatively correlated with OA severity. Using RNA sequencing, we identified that the upregulation of miR‐34a‐5p may be an important factor for the decrease in SESN2 expression. Further exploring the regulation mechanism of miR‐34a‐5p/SESN2 is of great significance for understanding the mechanism of DDH occurrence and development. Mechanistically, we showed that miR‐34a‐5p could significantly inhibit the expression of SESN2, thereby promoting the activity of the mTOR signaling pathway. We also found that miR‐34a‐5p significantly inhibited SESN2‐induced autophagy, thereby suppressing the proliferation and migration of chondrocytes. We further validated that knocking down miR‐34a‐5p in vivo resulted in a significant increase in SESN2 expression and autophagy activity in DDH‐OA cartilage. Our study suggests that miR‐34a‐5p is a negative regulator of DDH‐OA, and may provide a new target for the prevention of DDH‐OA.

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“…Several scholars have emphasized the substantial impact of circRNAs on the regulation of gene transcription by acting as miRNA sponges, boosting the expression of downstream mRNAs (31). A comprehensive interpretation of the role of epigenetically regulated miRNAs and the miRNA-mediated epigenetic modulation of genes is critical for understanding how aberrant miRNA expression might contribute to RA, and how this knowledge can be translated into diagnostic and therapeutic tool development (32).…”

Section: Discussionmentioning

confidence: 99%

Potential Role of circRNA-HIPK3/microRNA-124a Crosstalk in the Pathogenesis of Rheumatoid Arthritis

et al. 2022

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Background: Circular RNA-HIPK3 (CircHIPK3) has been shown to be aberrantly expressed in a variety of diseases, contributing to disease initiation and progression. The aim of the present study is to investigate the role of the circHIPK3 RNA/microRNA-124a interaction in the pathogenesis of rheumatoid arthritis (RA). Methods: This study included 79 RA patients and 30 control individuals. The patients involved were classified according to the disease activity score (DAS28) into mild (24 patients), moderate (24 patients), and severe (31 patients). Serum samples were collected to estimate the relative gene expression of circHIPK3 RNA and its target gene microRNA-124a by quantitative real time-PCR. Moreover, ELISA was used to detect the serum levels of monocyte chemoattractant protein-1 (MCP-1). Routine laboratory estimation of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and rheumatoid factor (RF) was also done. Results: In all grades of RA groups, there was a significantly substantial elevation of circHIPK3 RNA gene expression, with subsequent downregulation of miRNA-124a when compared to the control group. CircHIPK3 and microRNA-124a expression have been established to be inversely linked. Also, estimation of serum levels of MCP-1, ESR, CRP, and RF exhibited a significant increase in all grades of RA as compared to the control group. Conclusions: CircHIPK3 and microRNA-124a might be regarded as key players in the pathogenesis of RA. The cross-talk between them appears to be responsible for inducing joint inflammation by increasing MCP-1 production. Targeting circHIPK3 and microRNA-124a, and their downstream adaptor molecules, poses a new challenge for RA therapy.

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Promising diagnostic and therapeutic circRNAs for skeletal and chondral disorders

Cited by 17 publications

References 125 publications

Exosomal circFAM63Bsuppresses bone regeneration of postmenopausal osteoporosis via regulating miR‐578/HMGA2 axis

Exosomal circFAM63Bsuppresses bone regeneration of postmenopausal osteoporosis via regulating miR‐578/HMGA2 axis

MicroRNA‐34a‐5p promotes the progression of osteoarthritis secondary to developmental dysplasia of the hip by restraining SESN2‐induced autophagy

Potential Role of circRNA-HIPK3/microRNA-124a Crosstalk in the Pathogenesis of Rheumatoid Arthritis

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