Insights into coronary collateral formation from a novel porcine semiacute infarction model

Krackhardt, Florian; Harnoss, Jonathan M.; Waliszewski, Matthias; Ritter, Zully; Granzow, Susanne; Felsenberg, Dieter; Neumann, Konrad; Lerman, Lilian O.; Hillmeister, Philipp; Gebker, Rolf; Paetsch, Ingo; Riediger, Fabian; Bramlage, Peter; Buschmann, Ivo

doi:10.1097/mca.0000000000000569

Cited by 4 publications

(2 citation statements)

References 31 publications

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“…Coronary collateral development Belongs to microvascular circulatory disorders ,which is a supplying perfusion to ischemic tissue distal to an occluded segment [22,23]. An imbalance between pro-and antiangiogenic factors might lead to poor collateral growth [24,25].…”

Section: Discussionmentioning

confidence: 99%

Glycation of Apolipoprotein A-IV Impairs Angiogenesis Through The Orphan Nuclear Receptor Nur77

Liu¹,

Dai²,

Xu³

et al. 2021

Preprint

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Background Apo A-Ⅳ played an key role in Cardiovascular diseases, but the effect and mechanism of glycated apo A-Ⅳ on angiogenesis remains unclear. Methods In this study, we demonstrated that oral administration of glycated apoA-Ⅳ impaired blood perfusion recovery in a mouse hind-limb ischemia model. A reduction in blood perfusion recovery at day 21 was observed in the ischemic tissue of apoA-Ⅳ and glycated apoA-Ⅳ-treated mice. Results In this study, we demonstrated that glycated apo A-Ⅳ impaired blood perfusion recovery in a mouse hind-limb ischemia model. And in vitro study also showed that glycated apo A-Ⅳ inhibited the migration, proliferation, and tube-formation abilities of endothelial cells. Further research revealed that glycated apo A-Ⅳ regulated angiogenesis partly by interrupting Nur77. In addition, CML levels were increased in patients with Lower limb circulation (n = 30) compared with those with no limb circulation(n = 50). Conclusions We found impaired angiogenesis induced by glycated apo A-Ⅳ might contribute to poor coronary collateral growth by inhibit the expression of Nur77.

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Section: Discussionmentioning

confidence: 99%

Glycation of Apolipoprotein A-IV Impairs Angiogenesis Through The Orphan Nuclear Receptor Nur77

Liu¹,

Dai²,

Xu³

et al. 2021

Preprint

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show abstract

“…After the angiogram, an exchange guidewire was placed, and the guidewire was placed in the middle of the anterior descending branch of the coronary artery. Then the balloon was pressurized by 8–12 atm according to the difference of left anterior descending branch(LAD) vessel diameter, and the guidewire and balloon were withdrawn after 30 min to complete the reperfusion [ 12 , 13 ]. Finally, an electrocardiogram (ECG) was performed at 15 min postoperatively to assess the success of the model construction by ECG changes.…”

Section: Methodsmentioning

confidence: 99%

Shuangshen Ningxin capsule alleviates myocardial ischemia–reperfusion injury in miniature pigs by modulating mitophagy: network pharmacology and experiments in vivo

Jia,

Chen,

Xin

et al. 2023

Chin Med

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Background Myocardial ischemia/reperfusion injury (MI/RI) is involved in a variety of pathological states for which there is no effective treatment exists. Shuangshen Ningxin (SSNX) capsule which is developed by Xiyuan Hospital, Chinese Academy of Traditional Chinese Medicine has been demonstrated to alleviate MI/RI, but its mechanism remains to be further elucidated. Methods The MI/RI miniature pigs model was constructed to assess the pharmacodynamics of SSNX by blocking the proximal blood flow of the left anterior descending branch of the cardiac coronary artery through an interventional balloon. The principal chemical compounds and potential targets of SSNX were screened by HPLC–MS and SwissTargetPrediction. The targets of MI/RI were identified based on Online Mendelian Inheritance in Man (OMIM) and GeneCards. Cytoscape 3.9.0 was applied to construct a protein–protein interaction (PPI) network, and Gene Ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed using metascape. To further validate the mechanism of SSNX, Molecular docking, Transmission electron microscopy, and Western blot analysis were used to test the effectiveness of targets in related pathways. Results Our results indicated that SSNX significantly improved cardiac function, attenuated myocardial I/R injury. Through network analysis, a total of 15 active components and 201 targets were obtained from SSNX, 75 of which are potential targets for the treatment of MI/RI. KEGG and MCODE analysis showed that SSNX is involved in the mitophagy signaling pathway, and ginsenoside Rg1, ginsenoside Rb1 and ginsenoside Rb2 are key components associated with the mitophagy. Further experimental results proved that SSNX protected mitochondrial structure and function, and significantly reduced the expression of mitophagy-related proteins PTEN-induced putative kinase 1 (PINK1), Parkin, FUN14 domain containing 1 (FUNDC1) and Bcl-2/E1B-19 kDa interacting protein 3 (BNIP3) in MI/RI miniature pigs. Conclusion In our study, the integration of network pharmacology and experiments in vivo demonstrated that SSNX interfered with MI/RI by inhibiting mitophagy.

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Coronary collaterals in patients with ST-elevation myocardial infarction presenting late after symptom onset

et al. 2020

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Insights into coronary collateral formation from a novel porcine semiacute infarction model

Abstract: The confirmation of preformed coronary anastomoses during the process of collateralization (natural bypasses) offers a preclinical avenue to carry out arteriogenetic pharmaceutical research in patients with ischemic heart disease.

Cited by 4 publications

References 31 publications

Glycation of Apolipoprotein A-IV Impairs Angiogenesis Through The Orphan Nuclear Receptor Nur77

Glycation of Apolipoprotein A-IV Impairs Angiogenesis Through The Orphan Nuclear Receptor Nur77

Shuangshen Ningxin capsule alleviates myocardial ischemia–reperfusion injury in miniature pigs by modulating mitophagy: network pharmacology and experiments in vivo

Coronary collaterals in patients with ST-elevation myocardial infarction presenting late after symptom onset

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