Neuraminidase-1 promotes heart failure after ischemia/reperfusion injury by affecting cardiomyocytes and invading monocytes/macrophages

Heimerl, Maren; Sieve, Irina; Ricke‐Hoch, Melanie; Erschow, Sergej; Battmer, Karin; Scherr, Michaela; Hilfiker‐Kleiner, Denise

doi:10.1007/s00395-020-00821-z

Cited by 57 publications

(46 citation statements)

References 42 publications

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“…A mouse anti-troponin T (TnT) antibody (1:100; Millipore Corporation, Billerica, MA, United States) was used to label the cardiomyocytes and 4′,6-diamidino-2-phenylindole (DAPI; Beyotime) used to counterstain the nuclei. Images were captured with a fluorescence microscope (Olympus, Tokyo, Japan), and apoptosis was assessed based on the overlap between TnT and TUNEL staining ( Domingues et al, 2020 ; Heimerl et al, 2020 ).…”

Section: Methodsmentioning

confidence: 99%

RETRACTED: Mitofusin-2 Enhances Mitochondrial Contact With the Endoplasmic Reticulum and Promotes Diabetic Cardiomyopathy

Zhang

Wang

2021

Front. Physiol.

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Diabetic cardiomyopathy has been associated with mitochondrial damage. Mitochondria–endoplasmic reticulum (ER) contact is an important determinant of mitochondrial function and ER homeostasis. We therefore investigated whether hyperglycemia can damage the mitochondria by increasing their contact with the ER in cardiomyocytes. We found that hyperglycemia induced mitochondria–ER contact in cardiomyocytes, as evidenced by the increased MMM1, MDM34, and BAP31 expressions. Interestingly, the silencing of Mfn2 reduced the cooperation between the mitochondria and the ER in cardiomyocytes. Mfn2 silencing improved cardiomyocyte viability and function under hyperglycemic conditions. Additionally, the silencing of Mfn2 markedly attenuated the release of calcium from the ER to the mitochondria, thereby preserving mitochondrial metabolism in cardiomyocytes under hyperglycemic conditions. Mfn2 silencing reduced mitochondrial reactive oxygen species production, which reduced mitochondria-dependent apoptosis in hyperglycemia-treated cardiomyocytes. Finally, Mfn2 silencing attenuated ER stress in cardiomyocytes subjected to high-glucose stress. These results demonstrate that Mfn2 promotes mitochondria–ER contact in hyperglycemia-treated cardiomyocytes. The silencing of Mfn2 sustained mitochondrial function, suppressed mitochondrial calcium overload, prevented mitochondrial apoptosis, and reduced ER stress, thereby enhancing cardiomyocyte survival under hyperglycemic conditions.

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Section: Methodsmentioning

confidence: 99%

RETRACTED: Mitofusin-2 Enhances Mitochondrial Contact With the Endoplasmic Reticulum and Promotes Diabetic Cardiomyopathy

Zhang

Wang

2021

Front. Physiol.

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“…Its irreversible opening during IRI triggers cardiomyocyte necrosis rather than apoptosis [115]. mPTP remains closed during acute myocardial ischemia and opens within the first few minutes of reperfusion, allowing small molecules, which normally cannot cross the mitochondrial membranes, to pass through, thus, increasing the osmotic pressure of the mitochondrial matrix, inducing mitochondrial fragmentation, and releasing Cyt C [83,112,[116][117][118] (Figure 2).…”

Section: Enhanced Myocardial Ischemicmentioning

confidence: 99%

[Retracted] Protective Effect of Nicorandil on Cardiac Microvascular Injury: Role of Mitochondrial Integrity

Jiang

et al. 2021

Oxidative Medicine and Cellular Longevity

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A major shortcoming of postischemic therapy for myocardial infarction is the no-reflow phenomenon due to impaired cardiac microvascular function including microcirculatory barrier function, loss of endothelial activity, local inflammatory cell accumulation, and increased oxidative stress. Consequently, inadequate reperfusion of the microcirculation causes secondary ischemia, aggravating the myocardial reperfusion injury. ATP-sensitive potassium ion (KATP) channels regulate the coronary blood flow and protect cardiomyocytes from ischemia-reperfusion injury. Studies in animal models of myocardial ischemia-reperfusion have illustrated that the opening of mitochondrial KATP (mito-KATP) channels alleviates endothelial dysfunction and reduces myocardial necrosis. By contrast, blocking mito-KATP channels aggravates microvascular necrosis and no-reflow phenomenon following ischemia-reperfusion injury. Nicorandil, as an antianginal drug, has been used for ischemic preconditioning (IPC) due to its mito-KATP channel-opening effect, thereby limiting infarct size and subsequent severe ischemic insult. In this review, we analyze the protective actions of nicorandil against microcirculation reperfusion injury with a focus on improving mitochondrial integrity. In addition, we discuss the function of mitochondria in the pathogenesis of myocardial ischemia.

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“…GO [76], SLC16A9 [77], ACADSB (acyl-CoA dehydrogenase short/branched chain) [78], IMPA1 [79], CD300LG [80], CIRBP (cold inducible RNA binding protein) [81], PIK3R1 [82], YEATS4 [83], USP2 [84], NEDD9 [85], CHCHD5 [86] and ERAP1 [87] promotes hypertension. HSPB1 [88], CRYAB (crystallin alpha B) [89], ANXA5 [90], CCR2 [91], RGS4 [92], TNFRSF1A [93], XBP1 [94], NKX2-5 [95], NEU1 [96], GSTP1 [97], COMT (catechol-O-methyltransferase) [98], LIMK1 [99], CAMKK1 [100], CD276 [101], SMARCA4 [102], ADORA2B [103], ACOT1 [104], RGN (regucalcin) [105], PPA2 [106], KAT2B [107], PDK1 [108], CS (citrate synthase)…”

Section: Discussionmentioning

confidence: 99%

Identification of biomarkers, pathways and potential therapeutic targets for heart failure using bioinformatics analysis

Vastrad¹,

Vastrad²

2021

Preprint

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Heart failure (HF) is a complex cardiovascular diseases associated with high mortality. To discover key molecular changes in HF, we analyzed next-generation sequencing (NGS) data of HF. In this investigation, differentially expressed genes (DEGs) were analyzed using limma in R package from GSE161472 of the Gene Expression Omnibus (GEO). Then, gene enrichment analysis, protein-protein interaction (PPI) network, miRNA-hub gene regulatory network and TF-hub gene regulatory network construction, and topological analysis were performed on the DEGs by the Gene Ontology (GO), REACTOME pathway, STRING, HiPPIE, miRNet, NetworkAnalyst and Cytoscape. Finally, we performed receiver operating characteristic curve (ROC) analysis of hub genes. A total of 930 DEGs 9464 up regulated genes and 466 down regulated genes) were identified in HF. GO and REACTOME pathway enrichment results showed that DEGs mainly enriched in localization, small molecule metabolic process, SARS-CoV infections and the citric acid (TCA) cycle and respiratory electron transport. Subsequently, the PPI network, miRNA-hub gene regulatory network and TF-hub gene regulatory network were constructed, and 10 hub genes in these network were focused on by centrality analysis and module analysis. Furthermore, data showed that HSP90AA1, ARRB2, MYH9, HSP90AB1, FLNA, EGFR, PIK3R1, CUL4A, YEATS4 and KAT2B were good diagnostic values. In summary, this study suggests that HSP90AA1, ARRB2, MYH9, HSP90AB1, FLNA, EGFR, PIK3R1, CUL4A, YEATS4 and KAT2B may act as the key genes in HF.

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Neuraminidase-1 promotes heart failure after ischemia/reperfusion injury by affecting cardiomyocytes and invading monocytes/macrophages

Cited by 57 publications

References 42 publications

RETRACTED: Mitofusin-2 Enhances Mitochondrial Contact With the Endoplasmic Reticulum and Promotes Diabetic Cardiomyopathy

RETRACTED: Mitofusin-2 Enhances Mitochondrial Contact With the Endoplasmic Reticulum and Promotes Diabetic Cardiomyopathy

[Retracted] Protective Effect of Nicorandil on Cardiac Microvascular Injury: Role of Mitochondrial Integrity

Identification of biomarkers, pathways and potential therapeutic targets for heart failure using bioinformatics analysis

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