CircRNA Chordc1 protects mice from abdominal aortic aneurysm by contributing to the phenotype and growth of vascular smooth muscle cells

He, Xiang; Li, Xinzhong; Han, Yanming; Chen, Guojun; Xu, Tong; Cai, Donghua; Sun, Yili; Wang, Shifei; Lai, Yanxian; Teng, Zhonghua; Huang, Suming; Liao, Wangjun; Liao, Yulin; Bin, Jianping; Xiu, Jiancheng

doi:10.1016/j.omtn.2021.11.005

Cited by 24 publications

(14 citation statements)

References 39 publications

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“…CircChordc1 was found to be significantly deregulated in aneurysmal tissue compared to healthy arteries, and it was capable of converting VSMCs to a contractile phenotype and improving their growth by triggering waveform protein degeneration and boosting the GSK3/-catenin pathway, which inhibited aneurysm formation and minimized the chances of fracture in angiotensin II and CaCl2-induced AAA mouse models [ 72 ].…”

Section: Cardiovascular Diseases Associated With Vsmcs Phenotypic Swi...mentioning

confidence: 99%

Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases

Tang

Chen

Zhang

et al. 2022

Cells

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Vascular smooth muscle cells (VSMCs), the major cell type in the arterial vessel wall, have a contractile phenotype that maintains the normal vessel structure and function under physiological conditions. In response to stress or vascular injury, contractile VSMCs can switch to a less differentiated state (synthetic phenotype) to acquire the proliferative, migratory, and synthetic capabilities for tissue reparation. Imbalances in VSMCs phenotypic switching can result in a variety of cardiovascular diseases, including atherosclerosis, in-stent restenosis, aortic aneurysms, and vascular calcification. It is very important to identify the molecular mechanisms regulating VSMCs phenotypic switching to prevent and treat cardiovascular diseases with high morbidity and mortality. However, the key molecular mechanisms and signaling pathways participating in VSMCs phenotypic switching have still not been fully elucidated despite long-term efforts by cardiovascular researchers. In this review, we provide an updated summary of the recent studies and systematic knowledge of VSMCs phenotypic switching in atherosclerosis, in-stent restenosis, aortic aneurysms, and vascular calcification, which may help guide future research and provide novel insights into the prevention and treatment of related diseases.

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Section: Cardiovascular Diseases Associated With Vsmcs Phenotypic Swi...mentioning

confidence: 99%

Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases

Tang

Chen

Zhang

et al. 2022

Cells

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“…Arencibia et al showed that lncRNAs regulate VSMCPS and participate in the pathological process of in-stent stenosis ( Arencibia et al, 2022 ). Additionally, He et al showed that circChordc1 could suppress vascular remodeling and reverse pathological aortic aneurysm progression through optimized VSMCPS and improved their growth ( He et al, 2022 ). However, hitherto, no effective drugs targeting these non-coding RNA are available for clinical practice.…”

Section: Discussionmentioning

confidence: 99%

Global trends and Frontier topics about vascular smooth muscle cells phenotype switch: A bibliometric analysis from 1999 to 2021

et al. 2022

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Objective: Vascular smooth muscle cell phenotype switch (VSMCPS) plays a significant role in vascular remodeling. This study aimed to conduct a bibliometric analysis and visualize the knowledge map of research on VSMCPS.Methods: We retrieved publications focusing on VSMCPS from the Web of Science Core Collection database (SCI-EXPANDED) from 1999 to 2021. Using bibliometric tools, VOSviewer and CiteSpace, we identified the most productive researchers, journals, institutions, and countries. At the same time, the trends, hot topics, and knowledge networks were analyzed and visualized.Results: A total of 2213 publications were included in this analysis. The number of annual publications in the VSMCPS field exhibited an upward trend and could be roughly divided into three phases. Until 2006, the most prolific authors were from the United States. As of 2008, the number of articles published in China increased dramatically to reach 126 papers in 2020. As of 2014, China was the most productive country in this field. The United States ranked first in the number of highly-influential authors, institutions, and literature from 1999 to 2022. Owens GK, Hata, Akiko, and Wen, jin-kun were the most prolific authors. Arteriosclerosis Thrombosis and Vascular Biology, Circulation Research, and Cardiovascular Research were the top-ranked journals in this field. “Vascular remodeling,” “atherosclerosis,” “neointima,” “hypertension”, and “inflammation” were the main researched topics. New diseases, new mechanisms, and new phenotype (e.g., micro RNA, macrophage-like-cell, hypoxia, autophagy, long noncoding RNA, oxidative stress, endoplasmic reticulum stress, senescence, aging, abdominal aortic aneurysm, and aortic dissection) represent the trending topics in recent years.Conclusion: This study systematically analyzed and visualized the knowledge map of VSMCPS over the past 2 decades. Our findings provide a comprehensive overview for scholars who want to understand current trends and new research frontiers in this area.

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“…We next explored the relationship between ANXA2 and β-catenin pathway. A previous report showed that ANXA2 interacts with GSK3β in other organ (30). Hence, we tested whether ANXA2 could bind to GSK3β in renal tubular cells.…”

Section: Anxa2 Promotes Lysosomal Functions Through βCatenin/tcf4 Sig...mentioning

confidence: 95%

Annexin A2 plays a key role in protecting against acute kidney injury through β-catenin/TFEB pathway

Zhou

Shen

Miao

et al. 2022

Preprint

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Aim Acute kidney injury (AKI) is becoming a heavy health burden worldwide. There are no effective therapeutic strategies nowadays. Recent studies showed that autophagy and lysosome stabilization could inhibit tubular cell apoptosis, and protect against AKI. Annexin A2 (ANXA2), a calcium-regulated phospholipid-binding protein, was found to be highly involved in autophagy. However, its role in AKI has not been elucidated. Results We found that ANXA2 is highly increased in renal tubular cells in cisplatin-treated mice, and in the urine and kidney samples from AKI patients. Ectopic expression of ANXA2 promoted lysosomal functions and autophagic flux, and protected against tubular cell apoptosis in AKI mice. Transcriptome analysis further identified that ANXA2 was intimately correlated with lysosome biogenesis, autophagy, and β-catenin signaling. Mechanistically, ANXA2 induced β-catenin activation through binding to and inhibiting on GSK3β, which further triggered T cell factor 4 (TCF4)-mediated transcription factor EB (TFEB) signaling pathway. As a result, TFEB activation regulated lysosomal proteostasis and effectively promoted autophagic flux. This greatly protected against renal tubular cell apoptosis and alleviated AKI. Innovation: These findings underline ANXA2 serves as a new therapeutic potential for AKI which lacks effective treatment. Conclusion We demonstrated that ANXA2 plays a key role in retarding AKI, which is associated with its inductive effects on β-catenin/TFEB-induced lysosmal pathway.

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CircRNA Chordc1 protects mice from abdominal aortic aneurysm by contributing to the phenotype and growth of vascular smooth muscle cells

Cited by 24 publications

References 39 publications

Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases

Vascular Smooth Muscle Cells Phenotypic Switching in Cardiovascular Diseases

Global trends and Frontier topics about vascular smooth muscle cells phenotype switch: A bibliometric analysis from 1999 to 2021

Annexin A2 plays a key role in protecting against acute kidney injury through β-catenin/TFEB pathway

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