[Retracted] CircANXA2 Promotes Myocardial Apoptosis in Myocardial Ischemia‐Reperfusion Injury via Inhibiting miRNA‐133 Expression

Zong, Lei; Wang, Weixin

doi:10.1155/2020/8590861

Cited by 26 publications

(13 citation statements)

References 28 publications

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“…Moreover, the mechanism of RFS-related myocardial injury remains to be elucidated. It has been reported that CK-MB, LDH, and cTnI are markers of myocyte injury (34), and myocardial apoptosis is also a prognostic indicator of myocardial injury (35). Appearance of a reduction in cardiac contractility following a diffuse multifocal inflammatory infiltrate, myocardial fiber disorganization, cardiomyocyte apoptosis, and increased expression of CK-MB, LDH, and cTnI in our study indicated the occurrence of severe myocardial injury induced by SCR.…”

Section: Discussionsupporting

confidence: 60%

SIRT3-mediated mitochondrial autophagy in refeeding syndrome-related myocardial injury in sepsis rats

Li¹,

Lu²,

Zhang³

et al. 2022

Ann Transl Med

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Background: Myocardial injury induced by refeeding syndrome (RFS) is one of the important causes of deterioration in critically ill patients. Sirtuin-3 (SIRT3) has been shown to regulate mitochondrial autophagy in myocardial ischemia/reperfusion injury; however, the role of mitochondrial autophagy on RFS-related myocardial injury in patients in critical condition has not been reported on.Methods: Thirty Sprague-Dawley (SD) rats were divided into 3 groups (n=10 each group): the control group; the standard calorie refeeding (SCR) group; and the low calorie refeeding (LCR) group. The rats were weighed every third or four days from day 1 to day 14. On day 14, all rats were anesthetized and received an echocardiography test. Blood and bronchoalveolar lavage fluid (BALF) were collected and tested for arterial oxygen pressure (PaO 2 ), phosphorus (P), and calcium (Ca), creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and cardiac troponin 1 (cTnI), myeloperoxidase (MPO), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and IL-6. The histopathological change of hearts and lungs were evaluated, and lung injury score was calculated. Mitochondrial autophagy related proteins (including Beclin1, LC3, mitofusin-2, Mfn2, PINK1, Parkin, and SIRT3) were analyzed using a Western blot. To evaluate the effect of SIRT3, 20 rats were divided into 2 groups (n=10 each group): The adeno-associated virus 9 (AAV9-Nc) group; and the AAV9-SIRT3 overexpression (AAV9-SIRT3) group. The protocols for rats were the same as the SCR group since day 22 after injection of AAV9. The protein expressions of PINK1, Parkin, and SIRT3 were compared between the AAV9-Nc group and AAV9-SIRT3 group.Results: SCR caused significant decline in cardiac contractility and increased inflammatory cell infiltration in myocardial tissue. Meanwhile, Beclin1, LC3, PINK1, Parkin, and SIRT3 levels decreased, while Mfn2 showed no significant change. Furthermore, significant positive correlations were also found between SIRT3 and P, PINK1, and Parkin, and significant negative correlations were found between SIRT3 and CK-MB, LDH, and cTnI. Overexpression of SIRT3 activated the PINK1/Parkin mediated mitochondrial autophagy.Conclusions: SIRT3 has an essential role in RFS-related myocardial injury during LPS induced chronic sepsis in rats, probably via regulating mitochondrial autophagy.

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Section: Discussionsupporting

confidence: 60%

SIRT3-mediated mitochondrial autophagy in refeeding syndrome-related myocardial injury in sepsis rats

Li¹,

Lu²,

Zhang³

et al. 2022

Ann Transl Med

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“…Myocardial infarction is a severe disease associated with high mortality, and reestablishing the blood supply to the ischemic myocardial tissue is the most feasible treatment. However, prone to myocardial I/R injury is prone to occur [ 23 ]. Previous studies have shown that myocardial infarction prevention and treatment could target myocardial protective genes or deleterious genes or interfere with pathway gene expression, prompting the balance of protective genes and deleterious gene expression and regulating up- and downstream pathways [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

CTRP3 alleviates cardiac ischemia/reperfusion injury via LAMP1/JIP2/JNK signaling pathway

Song

Zhang

Wan

et al. 2022

Aging

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Background: C1q/tumor necrosis factor-related protein 3 (CTRP3) has been reported to be a crucial regulator in myocardial infarction. Nevertheless, the potential molecular mechanism of CTRP3 in ischemia/reperfusion (I/R) injury remains largely unclear. Methods: The cell model of myocardial I/R injury was established by oxygen-glucose deprivation/reoxygenation (OGD/R) of rat cardiomyocyte H9C2. Expression of CTRP3 and lysosomal-associated membrane protein 1 (LAMP1) was detected in H9C2 cells treated with oxygen-glucose deprivation/reoxygenation (OGD/R). H9C2 cells were transfected with overexpression plasmids of CTRP3 (pcDNA-CTRP3) and LAMP1 (pcDNA-LAMP1), or CTRP3 small interfering RNA (si-CTRP3) or/and pcDNA-LAMP1, and cell proliferation, apoptosis and oxidative stress were testified. Co-IP assay was performed to validate the relationship among CTRP3, LAMP1 and JIP2. The role of CTRP3 and LAMP1 in JIP2/JNK pathway was evaluated with Western blot assay. Furthermore, in vivo myocardial I/R injury model was constructed to investigate the effect of CTRP3. Results: Overexpression of CTRP3 and LAMP1 both significantly promoted cell proliferation, inhibited apoptosis and the production of reactive oxygen species (ROS), malondialdehyde (MAD) and cardiac troponin (cTn-I), while silencing CTRP3 exerted the opposite effects, and LAMP1 overexpression reversed the effect of silencing CTRP3 on the aspects above. CTRP3 interacted with LAMP1, and both CTRP3 and LAMP1 bound with JIP2. SP600125 (JNK inhibitor) could restore the effects of CTRP3 or LAMP1 overexpression on the expression of JIP2 and phosphorylated-JNK (p-JNK), proliferation and apoptosis. Moreover, overexpression of CTRP3 improved cardiac I/R injury in vivo . Conclusion: CTRP3 alleviates cardiac I/R injury by elevating LAMP1 and activating JIP2/JNK signaling pathway, which may serve as a potential therapeutic target for I/R injury.

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“…miRNA is an endogenous, single-stranded, non-coding, small regulatory RNA in a variety of eukaryotic cells ( Diaz et al, 2017 ). Studies have shown that miR-1275, miR-133, miR-148a and miR-324 interfere with the process of MIRI by inhibiting myocardial cell apoptosis, reducing myocardial inflammation, and promoting angiogenesis ( Dai et al, 2020 ; Jiang et al, 2020 ; Zong and Wang, 2020 ). lncRNA is a heterogeneous non-coding RNA that can directly regulate the transcription of target genes and the degradation of proteins ( Ruan et al, 2019 ).…”

Section: Mechanisms Of Myocardial Ischemia–reperfusion Injurymentioning

confidence: 99%

Saponins in Chinese Herbal Medicine Exerts Protection in Myocardial Ischemia–Reperfusion Injury: Possible Mechanism and Target Analysis

Wang

Zhou

et al. 2021

Front. Pharmacol.

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Myocardial ischemia is a high-risk disease among middle-aged and senior individuals. After thrombolytic therapy, heart tissue can potentially suffer further damage, which is called myocardial ischemia-reperfusion injury (MIRI). At present, the treatment methods and drugs for MIRI are scarce and cannot meet the current clinical needs. The mechanism of MIRI involves the interaction of multiple factors, and the current research hotspots mainly include oxidative stress, inflammation, calcium overload, energy metabolism disorders, pyroptosis, and ferroptosis. Traditional Chinese medicine (TCM) has multiple targets and few toxic side effects; clinical preparations containing Panax ginseng C. A. Mey., Panax notoginseng (Burk.) F. H. Chen, Aralia chinensis L., cardioprotection, and other Chinese herbal medicines have been used to treat patients with coronary heart disease, angina pectoris, and other cardiovascular diseases. Studies have shown that saponins are the main active substances in TCMs containing Panax ginseng C. A. Mey., Panax notoginseng (Burk.) F. H. Chen, Aralia chinensis L., and Radix astragali. In the present review, we sorted the saponin components with anti-MIRI effects and their regulatory mechanisms. Each saponin can play a cardioprotective role via multiple mechanisms, and the signaling pathways involved in different saponins are not the same. We found that more active saponins in Panax ginseng C. A. Mey. are mainly dammar-type structures and have a strong regulatory effect on energy metabolism. The highly active saponin components of Aralia chinensis L. are oleanolic acid structures, which have significant regulatory effects on calcium homeostasis. Therefore, saponins in Chinese herbal medicine provide a broad application prospect for the development of highly effective and low-toxicity anti-MIRI drugs.

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[Retracted] CircANXA2 Promotes Myocardial Apoptosis in Myocardial Ischemia‐Reperfusion Injury via Inhibiting miRNA‐133 Expression

Cited by 26 publications

References 28 publications

SIRT3-mediated mitochondrial autophagy in refeeding syndrome-related myocardial injury in sepsis rats

SIRT3-mediated mitochondrial autophagy in refeeding syndrome-related myocardial injury in sepsis rats

CTRP3 alleviates cardiac ischemia/reperfusion injury via LAMP1/JIP2/JNK signaling pathway

Saponins in Chinese Herbal Medicine Exerts Protection in Myocardial Ischemia–Reperfusion Injury: Possible Mechanism and Target Analysis

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