The protective effects of long non-coding RNA-ANCR on arterial calcification

Zhang, Xue; Chen, Jing; Meng, Qiang; Liu, Dong; Hu, Fangzhi; Zhu, Yuqing; Huang, Yewei; Liu, Yanan; Sun, Lin; Liang, Qiu-Hua

doi:10.1007/s00774-019-01076-y

Cited by 14 publications

(12 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Noncoding RNAs will be novel therapeutic genes for the treatment of vascular calcification in the future. Zhang et al 300 demonstrated that lncRNA-ANCR was an important factor regulating osteoblast differentiation. LncRNA-ANCR might significantly reduce the Runx2 and BMP2 expression and mineralized nodules formation by activating β-GP-induced VSMC autophagy, and weaken the VSMCs osteogenic differentiation, thereby protecting vascular calcification.…”

Section: Epigenetic Regulatory Mechanismsmentioning

confidence: 99%

Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials

Shi

Zhang

Huang

et al. 2022

Sig Transduct Target Ther

121

View full text Add to dashboard Cite

Epigenetics is closely related to cardiovascular diseases. Genome-wide linkage and association analyses and candidate gene approaches illustrate the multigenic complexity of cardiovascular disease. Several epigenetic mechanisms, such as DNA methylation, histone modification, and noncoding RNA, which are of importance for cardiovascular disease development and regression. Targeting epigenetic key enzymes, especially the DNA methyltransferases, histone methyltransferases, histone acetylases, histone deacetylases and their regulated target genes, could represent an attractive new route for the diagnosis and treatment of cardiovascular diseases. Herein, we summarize the knowledge on epigenetic history and essential regulatory mechanisms in cardiovascular diseases. Furthermore, we discuss the preclinical studies and drugs that are targeted these epigenetic key enzymes for cardiovascular diseases therapy. Finally, we conclude the clinical trials that are going to target some of these processes.

show abstract

Section: Epigenetic Regulatory Mechanismsmentioning

confidence: 99%

Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials

Shi

Zhang

Huang

et al. 2022

Sig Transduct Target Ther

121

View full text Add to dashboard Cite

show abstract

“…Liang, et al proved that long non‑coding RNA‑ANCR promoted the expression of LC3 and Atg5 in β‑GP‑induced VSMCs, and inhibited osteoblastic differentiation of VSMCs. The ANCR may attenuate arterial calcification through activating autophagy that inhibits osteogenic differentiation of VSMCs [ 40 ]. The autophagy inhibitor 3-MA or knockout of Atg5 increased calcium deposition, whereas the autophagy inducer valproic acid reduced VSMC calcification [ 31 ].…”

Section: Autophagy Affects Vascular Calcification By Interfering With the Osteogenic Differentiation Of Vsmcsmentioning

confidence: 99%

“…Keywords: Vascular calcification, Autophagy/mitophagy, Osteoblastic differentiation of VSMCs, Osteogenesis, AMPK/ mTOR, HIF-1a/PDK4, EphrinB2, GAS6/AXL differentiation of VSMCs. The ANCR may attenuate arterial calcification through activating autophagy that inhibits osteogenic differentiation of VSMCs [40]. The autophagy inhibitor 3-MA or knockout of Atg5 increased calcium deposition, whereas the autophagy inducer valproic acid reduced VSMC calcification [31].…”

Section: Autophagy Reduces Calcification By Inhibiting the Osteogenic Differentiation Of Vsmcsmentioning

confidence: 99%

Multiple functions of autophagy in vascular calcification

Zhou

Yuan

et al. 2021

Cell Biosci

View full text Add to dashboard Cite

Background Vascular calcification is a closely linked to cardiovascular diseases, such as atherosclerosis, chronic kidney disease, diabetes, hypertension and aging. The extent of vascular calcification is closely correlate with adverse clinical events and cardiovascular all-cause mortality. The role of autophagy in vascular calcification is complex with many mechanistic unknowns. Methods In this review, we analyze the current known mechanisms of autophagy in vascular calcification and discuss the theoretical advantages of targeting autophagy as an intervention against vascular calcification. Results Here we summarize the functional link between vascular calcification and autophagy in both animal models of and human cardiovascular disease. Firstly, autophagy can reduce calcification by inhibiting the osteogenic differentiation of VSMCs related to ANCR, ERα, β-catenin, HIF-1a/PDK4, p62, miR-30b, BECN1, mTOR, SOX9, GHSR/ERK, and AMPK signaling. Conversely, autophagy can induce osteoblast differentiation and calcification as mediated by CREB, degradation of elastin, and lncRNA H19 and DUSP5 mediated ERK signaling. Secondly, autophagy also links apoptosis and vascular calcification through AMPK/mTOR/ULK1, Wnt/β-catenin and GAS6/AXL synthesis, as apoptotic cells become the nidus for calcium-phosphate crystal deposition. The failure of mitophagy can activate Drp1, BNIP3, and NR4A1/DNA‑PKcs/p53 mediated intrinsic apoptotic pathways, which have been closely linked to the formation of vascular calcification. Additionally, autophagy also plays a role in osteogenesis by regulating vascular calcification, which in turn regulates expression of proteins related to bone development, such as osteocalcin, osteonectin, etc. and regulated by mTOR, EphrinB2 and RhoA. Furthermore, autophagy also promotes vitamin K2-induced MC3T3 E1 osteoblast differentiation and FGFR4/FGF18- and JNK/complex VPS34–beclin-1-related bone mineralization via vascular calcification. Conclusion The interaction between autophagy and vascular calcification are complicated, with their interaction affected by the disease process, anatomical location, and the surrounding microenvironment. Autophagy activation in existent cellular damage is considered protective, while defective autophagy in normal cells result in apoptotic activation. Identifying and maintaining cells at the delicate line between these two states may hold the key to reducing vascular calcification, in which autophagy associated clinical strategy could be developed.

show abstract

“…Therefore, the authors stated that miRNA30b protects against VCN by promoting autophagy through inhibition of Sox9 and mTOR [ 68 ]. Moreover, overexpression of anti-differentiation non-coding RNA (ANCR) induced autophagy, characterized by an increase in Atg5, LC3-I and LC3-II, and attenuated VCN both in vitro and in vivo [ 69 ]. Klotho knockout mice revealed age-related VCN, while beclin1 overexpression rescued Klotho knockout-induced VCN [ 70 ].…”

Section: Resultsmentioning

confidence: 99%

“…However, this ratio is rather unreliable and current guidelines on quantification of autophagic flux do not recommend the use of LC3-II/LC3-I ratios as a sole predictor of autophagic flux [ 95 ]. Furthermore, oestrogen, ANCR and atorvastatin have been demonstrated to enhance Atg5 expression and miRNA-30b has been shown to induce Beclin1 [ 66 , 67 , 68 , 69 ]. Only one study [ 71 ] determined autophagic flux (i.e., the turnover of LC3-II) by using an autophagy inhibitor, as is indicated in the most recent guidelines on the evaluation of autophagy [ 95 ].…”

Section: Discussionmentioning

confidence: 99%

The Protective Effects of the Autophagic and Lysosomal Machinery in Vascular and Valvular Calcification: A Systematic Review

Neutel

Hendrickx

Martinet

et al. 2020

IJMS

View full text Add to dashboard Cite

Background: Autophagy is a highly conserved catabolic homeostatic process, crucial for cell survival. It has been shown that autophagy can modulate different cardiovascular pathologies, including vascular calcification (VCN). Objective: To assess how modulation of autophagy, either through induction or inhibition, affects vascular and valvular calcification and to determine the therapeutic applicability of inducing autophagy. Data sources: A systematic review of English language articles using MEDLINE/PubMed, Web of Science (WoS) and the Cochrane library. The search terms included autophagy, autolysosome, mitophagy, endoplasmic reticulum (ER)-phagy, lysosomal, calcification and calcinosis. Study characteristics: Thirty-seven articles were selected based on pre-defined eligibility criteria. Thirty-three studies (89%) studied vascular smooth muscle cell (VSMC) calcification of which 27 (82%) studies investigated autophagy and six (18%) studies lysosomal function in VCN. Four studies (11%) studied aortic valve calcification (AVCN). Thirty-four studies were published in the time period 2015–2020 (92%). Conclusion: There is compelling evidence that both autophagy and lysosomal function are critical regulators of VCN, which opens new perspectives for treatment strategies. However, there are still challenges to overcome, such as the development of more selective pharmacological agents and standardization of methods to measure autophagic flux.

show abstract

The protective effects of long non-coding RNA-ANCR on arterial calcification

Cited by 14 publications

References 29 publications

Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials

Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials

Multiple functions of autophagy in vascular calcification

The Protective Effects of the Autophagic and Lysosomal Machinery in Vascular and Valvular Calcification: A Systematic Review

Contact Info

Product

Resources

About