MicroRNA-20b Promotes Cardiac Hypertrophy by the Inhibition of Mitofusin 2-Mediated Inter-organelle Ca2+ Cross-Talk

Qiu, Yue; Cheng, Rongchao; Liang, Chaoqi; Yao, Yuan; Zhang, Wenhao; Zhang, Jie; Zhang, Mingyu; Li, Bai‐Yan; Xu, Chaoqian; Zhang, Rong

doi:10.1016/j.omtn.2020.01.017

Cited by 35 publications

(29 citation statements)

References 50 publications

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“…Mitochondria are the powerhouse of oxidative phosphorylation in eukaryotes [ 20 ], wherein carbohydrates, fats, and proteins are oxidized and catabolized to produce energy [ 21 , 22 ]. Pyruvate is hydrolyzed to form triacyl acid and pyruvic acid in the mitochondria.…”

Section: Introductionmentioning

confidence: 99%

[Retracted] Puerarin Attenuates LPS‐Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control

Chang

Zhang

Dong

et al. 2021

Oxidative Medicine and Cellular Longevity

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Atherosclerosis is closely associated with the inflammatory reaction of vascular endothelial cells. Puerarin (Pue), the main active component isolated from the rhizome of Pueraria lobata, is an isoflavone compound with potent antioxidant properties. Although Pue exhibits promising antiatherosclerotic pharmacological effects, only a few studies have reported its protective effect on endothelial cells. This study found that Pue could partly regulate mitochondrial function in human umbilical vein endothelial cells (HUVECs) and reduce or inhibit lipopolysaccharide-induced inflammatory reactions and oxidative stress injury in HUVECs, likely via mitochondrial quality control. Furthermore, the protective effect of Pue on HUVECs was closely related to the SIRT-1 signaling pathway. Pue increased autophagy and mitochondrial antioxidant potential via increased SIRT-1 expression, reducing excessive production of ROS and inhibiting the expression of inflammatory factors and oxidative stress injury. Therefore, Pue may improve mitochondrial respiratory function and energy metabolism, increasing the vulnerability of HUVECs to an inflammatory state.

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Section: Introductionmentioning

confidence: 99%

[Retracted] Puerarin Attenuates LPS‐Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control

Chang

Zhang

Dong

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…These findings reported in this review indicate the major role of mitochondrial fission in pathological cardiac remodeling. In addition, a recent study showed that microRNA-20b intensified cardiac hypertrophy by downregulating Mfn2 and promoting cytoplasmic Ca 2+ overloading, weakening mitochondrial buffering capacity [ 63 ].…”

Section: Mitochondrial Dynamics and Cardiovascular Diseasementioning

confidence: 99%

[Retracted] Novel Insights into the Molecular Features and Regulatory Mechanisms of Mitochondrial Dynamic Disorder in the Pathogenesis of Cardiovascular Disease

Tan

Xia

et al. 2021

Oxidative Medicine and Cellular Longevity

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Mitochondria maintain mitochondrial homeostasis through continuous fusion and fission, that is, mitochondrial dynamics, which is precisely mediated by mitochondrial fission and fusion proteins, including dynamin-related protein 1 (Drp1), mitofusin 1 and 2 (Mfn1/2), and optic atrophy 1 (OPA1). When the mitochondrial fission and fusion of cardiomyocytes are out of balance, they will cause their own morphology and function disorders, which damage the structure and function of the heart, are involved in the occurrence and progression of cardiovascular disease such as ischemia-reperfusion injury (IRI), septic cardiomyopathy, and diabetic cardiomyopathy. In this paper, we focus on the latest findings regarding the molecular features and regulatory mechanisms of mitochondrial dynamic disorder in cardiovascular pathologies. Finally, we will address how these findings can be applied to improve the treatment of cardiovascular disease.

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“…These advantages also make AAV a popular delivery method of miRNA either in mechanistic studies or therapeutic effects on cardiovascular diseases. 3 , 7 , 8 , 13 , 14 , 15 …”

Section: Discussionmentioning

confidence: 99%

“… 1 Mitochondrial biogenesis, metabolic reprogramming (changes in fatty acid oxidation [FAO] and glycolysis pathway), mitochondrial oxidative stress, and oxidative phosphorylation (OXPHOS) have been shown to associated with pathological cardiac hypertrophy. 2 , 3 , 4 , 5 , 6 …”

Section: Introductionmentioning

confidence: 99%

“…Growing evidence has shown that miRNAs play important roles in the progression of cardiac hypertrophy 7 , 8 , 9 , 10 and they can regulate cardiac mitochondrial dysfunction, which results in pathological cardiac hypertrophy and heart failure (HF). 2 , 3 , 4 , 6 , 11 The manipulation of these miRNAs can be a therapeutic strategy to treat cardiac hypertrophy. However, common chemically modified miRNAs, such as miRNA agomirs/antagomirs, miRNA mimics, and miRNA sponges, have transient lifespans with short-term effects and require large-dose and repetitive delivery.…”

Section: Introductionmentioning

confidence: 99%

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Adeno-associated virus-mediated delivery of anti-miR-199a tough decoys attenuates cardiac hypertrophy by targeting PGC-1alpha

Yan

Wang

Zhu

et al. 2021

Molecular Therapy - Nucleic Acids

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MicroRNAs (miRNAs) are important regulators in the process of cardiac hypertrophy and heart failure. Previous studies have shown that miR-199a is upregulated in pressure-overload cardiac hypertrophy and that inhibition of miR-199a attenuates cardiac hypertrophy in vitro . However, the therapeutic role of anti-miR-199a treatment in the cardiac hypertrophy in vivo model is less known. Here, we show an efficient and useful method to treat mouse cardiac hypertrophy and restore cardiac function through injection of adeno-associated virus (AAV)-mediated anti-miR-199a tough decoys (TuDs). RNA-seq transcriptome analysis indicated that genes related to cytoplasmic translation and mitochondrial respiratory chain complex assembly were upregulated in anti-miR-199a-treated recovered hearts. We further validated that PGC-1α is the direct target of miR-199a involved in the therapeutic effect and the regulation of the PGC-1α/ERRα axis and that the downstream pathway of mitochondrial fatty acid oxidation and oxidative phosphorylation constitute the underlying mechanism of the restored mitochondrial structure and function in our anti-miR-199a-treated mice. Our study highlights the important regulatory role of miR-199a in cardiac hypertrophy and the value of the AAV-mediated miRNA delivery system.

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MicroRNA-20b Promotes Cardiac Hypertrophy by the Inhibition of Mitofusin 2-Mediated Inter-organelle Ca2+ Cross-Talk

Cited by 35 publications

References 50 publications

[Retracted] Puerarin Attenuates LPS‐Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control

[Retracted] Puerarin Attenuates LPS‐Induced Inflammatory Responses and Oxidative Stress Injury in Human Umbilical Vein Endothelial Cells through Mitochondrial Quality Control

[Retracted] Novel Insights into the Molecular Features and Regulatory Mechanisms of Mitochondrial Dynamic Disorder in the Pathogenesis of Cardiovascular Disease

Adeno-associated virus-mediated delivery of anti-miR-199a tough decoys attenuates cardiac hypertrophy by targeting PGC-1alpha

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