Pub Date : 2023-01-01DOI: 10.1097/CP9.0000000000000044
Yongjing Jiang, Gaoliang Zhou, Jun Feng, Likun Ma, Jianyuan Pan
Background and purpose: Risk factors that could be used to assess early and further improve the positive predictive value of blunt cardiac injury (BCI) are still inconclusive. We conducted a meta-analysis to quantitatively analyze the injury mechanism, risk factors, and outcomes associated with BCI in trauma patients. Methods: This systematic review and meta-analysis were performed to gather data on trauma patients with blunt cardiac injury. PubMed, Web of Science, and EMBASE databases were searched for studies until 20th November 2021. A pooled meta-analysis of injury mechanisms, risk factors, and outcomes concerning BCI was conducted. Results: We screened 256 records from which 11 studies published from 2000 to 2019 reporting 68,039 patients with trauma were included. Motor vehicle crash was the main injury mechanism, accounting for 65.2% of the attributed mechanisms for BCI [pool proportion = 0.652 (0.595–0.709)]. The pooled relative risks (RRs) revealed that patients with sternal fracture, shock on arrival, and history of cardiac disease were associated with increased risk of BCI (for sternal fracture: RR = 7.21 [95% confidence interval (CI) = 3.99–13.05]; for the shock on arrival: RR = 2.45, 95% CI = 2.12–2.84; for the history of cardiac disease: RR = 1.87, 95% CI = 1.11–3.16). A significant difference was observed in the length of stay between the BCI group compared to the no BCI group, 11.68 (95% CI = 8.79–14.58 days) vs. 20.46 (95% CI = 16.78–24.14 days). The risk of mortality was significantly higher in trauma patients with BCI as compared to those without BCI (RR = 1.70, 95% CI = 1.53–1.90). Conclusions: BCI was associated with increased mortality in our study. Patients also tended towards a longer length of stay. In addition to electrocardiogram and TnI, we recommend screening for BCI when trauma patients are in the presence of sternal fracture, shock, and a history of cardiac disease.
背景和目的：可用于早期评估并进一步提高钝性心脏损伤（BCI）阳性预测价值的风险因素尚不确定。我们进行了一项荟萃分析，以定量分析创伤患者脑机接口的损伤机制、危险因素和结果。方法：本系统综述和荟萃分析旨在收集外伤性心脏钝性损伤患者的数据。PubMed、Web of Science和EMBASE数据库在2021年11月20日之前一直在搜索研究。对脑机接口损伤机制、危险因素和结果进行了汇总荟萃分析。结果：我们筛选了256份记录，其中包括2000年至2019年发表的11项研究，报告了68039名创伤患者。机动车碰撞是主要的损伤机制，占脑机接口归因机制的65.2%[综合比例=0.652（0.595–0.709）]。综合相对风险（RR）显示，胸骨骨折、到达时休克、，心脏病史与脑机接口风险增加相关（胸骨骨折：RR=7.21[95%置信区间（CI）=3.99-13.05]；对于到达时的冲击：RR=2.45，95%CI=2.12-2.84；心脏病史：RR=1.87，95%CI=1.11–3.16）。与无脑机接口组相比，脑机接口治疗组的住院时间有显著差异，分别为11.68（95%CI=8.79–14.58天）和20.46（95%CI=16.78–24.14天）。有脑机接口的创伤患者的死亡率明显高于无脑机接口患者（RR=1.70，95%CI=1.53-1.90）。结论：在我们的研究中，脑机接口与死亡率增加有关。患者也倾向于延长住院时间。除了心电图和TnI外，当创伤患者存在胸骨骨折、休克和心脏病史时，我们建议对脑机接口进行筛查。
{"title":"Injury mechanism, risk factors and outcomes associated with blunt cardiac injury: a systematic review and meta-analysis","authors":"Yongjing Jiang, Gaoliang Zhou, Jun Feng, Likun Ma, Jianyuan Pan","doi":"10.1097/CP9.0000000000000044","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000044","url":null,"abstract":"Background and purpose: Risk factors that could be used to assess early and further improve the positive predictive value of blunt cardiac injury (BCI) are still inconclusive. We conducted a meta-analysis to quantitatively analyze the injury mechanism, risk factors, and outcomes associated with BCI in trauma patients. Methods: This systematic review and meta-analysis were performed to gather data on trauma patients with blunt cardiac injury. PubMed, Web of Science, and EMBASE databases were searched for studies until 20th November 2021. A pooled meta-analysis of injury mechanisms, risk factors, and outcomes concerning BCI was conducted. Results: We screened 256 records from which 11 studies published from 2000 to 2019 reporting 68,039 patients with trauma were included. Motor vehicle crash was the main injury mechanism, accounting for 65.2% of the attributed mechanisms for BCI [pool proportion = 0.652 (0.595–0.709)]. The pooled relative risks (RRs) revealed that patients with sternal fracture, shock on arrival, and history of cardiac disease were associated with increased risk of BCI (for sternal fracture: RR = 7.21 [95% confidence interval (CI) = 3.99–13.05]; for the shock on arrival: RR = 2.45, 95% CI = 2.12–2.84; for the history of cardiac disease: RR = 1.87, 95% CI = 1.11–3.16). A significant difference was observed in the length of stay between the BCI group compared to the no BCI group, 11.68 (95% CI = 8.79–14.58 days) vs. 20.46 (95% CI = 16.78–24.14 days). The risk of mortality was significantly higher in trauma patients with BCI as compared to those without BCI (RR = 1.70, 95% CI = 1.53–1.90). Conclusions: BCI was associated with increased mortality in our study. Patients also tended towards a longer length of stay. In addition to electrocardiogram and TnI, we recommend screening for BCI when trauma patients are in the presence of sternal fracture, shock, and a history of cardiac disease.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"53 - 62"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47638817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1097/CP9.0000000000000035
Yu Zhang, Junchu Tu, Yujie Li, Yanli Wang, Lin Lu, Chengjie Wu, Xi-Yong Yu, Yangxin Li
Cardiovascular diseases (CVDs) have high morbidity. Many endogenous and exogenous factors provoke the innate immune response causing tissue damage and accelerating the progression of the diseases. The macrophages are the major cells mediating the inflammatory response. Inflammasomes are multi-protein complexes that recognize danger signals, activate cytokines, and participate in the inflammatory response. Both macrophages and inflammasomes play a critical role in the development and progression of CVDs, such as myocardial infarction, hypertension, and atherosclerosis. This review will summarize the studies on macrophages and inflammasomes and discuss potential therapeutic interventions. Moreover, macrophages and inflammasomes play distinct role in the inflammation process, but closely linked. The inflammasome system occur in macrophages, and macrophage pyroptosis may be provoked by inflammasome activation. The cytokines secreted by macrophages may be related to the activation of inflammasomes, and further activate macrophages in the heart and cause the interconversion of M1 phenotype and M2 phenotype. The mechanism of inflammasomes regulating macrophage polarization remains to be further investigated.
{"title":"Inflammation macrophages contribute to cardiac homeostasis","authors":"Yu Zhang, Junchu Tu, Yujie Li, Yanli Wang, Lin Lu, Chengjie Wu, Xi-Yong Yu, Yangxin Li","doi":"10.1097/CP9.0000000000000035","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000035","url":null,"abstract":"Cardiovascular diseases (CVDs) have high morbidity. Many endogenous and exogenous factors provoke the innate immune response causing tissue damage and accelerating the progression of the diseases. The macrophages are the major cells mediating the inflammatory response. Inflammasomes are multi-protein complexes that recognize danger signals, activate cytokines, and participate in the inflammatory response. Both macrophages and inflammasomes play a critical role in the development and progression of CVDs, such as myocardial infarction, hypertension, and atherosclerosis. This review will summarize the studies on macrophages and inflammasomes and discuss potential therapeutic interventions. Moreover, macrophages and inflammasomes play distinct role in the inflammation process, but closely linked. The inflammasome system occur in macrophages, and macrophage pyroptosis may be provoked by inflammasome activation. The cytokines secreted by macrophages may be related to the activation of inflammasomes, and further activate macrophages in the heart and cause the interconversion of M1 phenotype and M2 phenotype. The mechanism of inflammasomes regulating macrophage polarization remains to be further investigated.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"6 - 17"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44936686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01Epub Date: 2023-04-04DOI: 10.1097/CP9.0000000000000038
Yan Shen, Il-Man Kim, Neal L Weintraub, Yaoliang Tang
The metabolic status of surviving cardiomyocytes (CM) in the myocardial tissues of patients who sustained myocardial infarction (MI) is largely unknown. Spatial single-cell RNA-sequencing (scRNA-seq) is a novel tool that enables the unbiased analysis of RNA signatures within intact tissues. We employed this tool to assess the metabolic profiles of surviving CM in the myocardial tissues of patients post-MI.
Methods: A spatial scRNA-seq dataset was used to compare the genetic profiles of CM from patients with MI and control patients; we analyzed the metabolic adaptations of surviving CM within the ischemic niche. A standard pipeline in Seurat was used for data analysis, including normalization, feature selection, and identification of highly variable genes using principal component analysis (PCA). Harmony was used to remove batch effects and integrate the CM samples based on annotations. Uniform manifold approximation and projection (UMAP) was used for dimensional reduction. The Seurat "FindMarkers" function was used to identify differentially expressed genes (DEGs), which were analyzed by the Gene Ontology (GO) enrichment pathway. Finally, the scMetabolism R tool pipeline with parameters method = VISION (Vision is a flexible system that utilizes a high-throughput pipeline and an interactive web-based report to annotate and explore scRNA-seq datasets in a dynamic manner) and metabolism.type = Kyoto Encyclopedia of Genes and Genomes (KEGG) was used to quantify the metabolic activity of each CM.
Results: Analysis of spatial scRNA-seq data showed fewer surviving CM in infarcted hearts than in control hearts. GO analysis revealed repressed pathways in oxidative phosphorylation, cardiac cell development, and activated pathways in response to stimuli and macromolecular metabolic processes. Metabolic analysis showed downregulated energy and amino acid pathways and increased purine, pyrimidine, and one-carbon pool by folate pathways in surviving CM.
Conclusions: Surviving CM within the infarcted myocardium exhibited metabolic adaptations, as evidenced by the downregulation of most pathways linked to oxidative phosphorylation, glucose, fatty acid, and amino acid metabolism. In contrast, pathways linked to purine and pyrimidine metabolism, fatty acid biosynthesis, and one-carbon metabolism were upregulated in surviving CM. These novel findings have implications for the development of effective strategies to improve the survival of hibernating CM within the infarcted heart.
心肌梗死（MI）患者心肌组织中存活心肌细胞（CM）的代谢状况在很大程度上是未知的。空间单细胞RNA测序（scRNA-seq）是一种新的工具，能够对完整组织内的RNA特征进行无偏分析。我们使用该工具评估MI后患者心肌组织中存活CM的代谢谱。方法：使用空间scRNA-seq数据集比较MI患者和对照患者CM的遗传谱；我们分析了存活的CM在缺血生态位内的代谢适应。Seurat中的标准管道用于数据分析，包括归一化、特征选择和使用主成分分析（PCA）识别高度可变基因。Harmony用于消除批量效应，并基于注释集成CM样本。统一流形近似和投影（UMAP）用于降维。Seurat“FindMarkers”功能用于鉴定差异表达基因（DEG），通过基因本体论（GO）富集途径对其进行分析。最后scMetabolism R工具管道的参数方法=VISION（VISION是一个灵活的系统，它利用高通量管道和交互式网络报告以动态方式注释和探索scRNA-seq数据集）和metabolism.type=Kyoto Encyclopedia of Genes and Genomes（KEGG）来量化每个CM的代谢活性数据显示梗死心脏中存活的CM少于对照心脏。GO分析揭示了氧化磷酸化、心脏细胞发育中被抑制的途径，以及刺激和大分子代谢过程中被激活的途径。代谢分析显示，在存活的CM中，能量和氨基酸途径下调，嘌呤、嘧啶和一个碳库被叶酸途径增加。结论：梗死心肌中存活的CM表现出代谢适应，与氧化磷酸化、葡萄糖、脂肪酸和氨基酸代谢相关的大多数途径下调就是明证。相反，在存活的CM中，与嘌呤和嘧啶代谢、脂肪酸生物合成和单碳代谢相关的途径被上调。这些新发现对开发有效策略以提高梗死心脏内冬眠CM的存活率具有启示意义。
{"title":"Identification of the metabolic state of surviving cardiomyocytes in the human infarcted heart by spatial single-cell transcriptomics.","authors":"Yan Shen, Il-Man Kim, Neal L Weintraub, Yaoliang Tang","doi":"10.1097/CP9.0000000000000038","DOIUrl":"10.1097/CP9.0000000000000038","url":null,"abstract":"<p><p>The metabolic status of surviving cardiomyocytes (CM) in the myocardial tissues of patients who sustained myocardial infarction (MI) is largely unknown. Spatial single-cell RNA-sequencing (scRNA-seq) is a novel tool that enables the unbiased analysis of RNA signatures within intact tissues. We employed this tool to assess the metabolic profiles of surviving CM in the myocardial tissues of patients post-MI.</p><p><strong>Methods: </strong>A spatial scRNA-seq dataset was used to compare the genetic profiles of CM from patients with MI and control patients; we analyzed the metabolic adaptations of surviving CM within the ischemic niche. A standard pipeline in Seurat was used for data analysis, including normalization, feature selection, and identification of highly variable genes using principal component analysis (PCA). Harmony was used to remove batch effects and integrate the CM samples based on annotations. Uniform manifold approximation and projection (UMAP) was used for dimensional reduction. The Seurat \"FindMarkers\" function was used to identify differentially expressed genes (DEGs), which were analyzed by the Gene Ontology (GO) enrichment pathway. Finally, the scMetabolism R tool pipeline with parameters method = VISION (Vision is a flexible system that utilizes a high-throughput pipeline and an interactive web-based report to annotate and explore scRNA-seq datasets in a dynamic manner) and metabolism.type = Kyoto Encyclopedia of Genes and Genomes (KEGG) was used to quantify the metabolic activity of each CM.</p><p><strong>Results: </strong>Analysis of spatial scRNA-seq data showed fewer surviving CM in infarcted hearts than in control hearts. GO analysis revealed repressed pathways in oxidative phosphorylation, cardiac cell development, and activated pathways in response to stimuli and macromolecular metabolic processes. Metabolic analysis showed downregulated energy and amino acid pathways and increased purine, pyrimidine, and one-carbon pool by folate pathways in surviving CM.</p><p><strong>Conclusions: </strong>Surviving CM within the infarcted myocardium exhibited metabolic adaptations, as evidenced by the downregulation of most pathways linked to oxidative phosphorylation, glucose, fatty acid, and amino acid metabolism. In contrast, pathways linked to purine and pyrimidine metabolism, fatty acid biosynthesis, and one-carbon metabolism were upregulated in surviving CM. These novel findings have implications for the development of effective strategies to improve the survival of hibernating CM within the infarcted heart.</p>","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"18-26"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7d/ed/cp9-8-18.PMC10180026.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10301091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1097/CP9.0000000000000042
Ida Nađ, Dorotea Šijak, A. Miculinić, D. Bartoniček, Maja Hrabak Paar, I. Malcic
Scimitar syndrome is a rare congenital heart defect (CHD) manifested by a partial abnormal inflow of pulmonary veins of the right lung into the suprahepatic segment of the inferior vena cava (VCI), making an angiographic image with the right heart edge similar to a Turkish saber (“scimitar”). It is found in only 1 to 3 per 100,000 births. Here we are presenting a patient who, in addition to the basic finding and presentation of a special partial anomalous inflow of pulmonary veins, also had other features of the Scimitar syndrome; dextroposition of the heart, without signs of heterotaxy, hypoplasia of the right lung, aberrant arterial supply of the right lung from the descending aorta (lung sequestration) with all hemodynamic signs of left-right flow (dilated right heart cavity and pulmonary artery), but without pulmonary hypertension. In addition, the patient had esophageal atresia with distal tracheoesophageal fistula (TEF). Treatment included operative occlusion of TEF with termino-terminal esophageal anastomosis. In the further course, esophagography revealed circular esophageal stenosis at the anastomosis site, but without the need for dilatation, which resolved spontaneously. Tracheotomy was needed due to the inability to separate from mechanical ventilation. Considering cardiopulmonary stability and the absence of pulmonary hypertension, a complete cardiosurgical correction was postponed to after the first year of life. The review is exceptional due to the concomitant occurrence of a TEF Vogt type IIIb, because the unusual combination of Scimitar syndrome with such type of TEF has not been described in the literature so far. To our knowledge, there is only one described case report with an H-type of TEF.
{"title":"Scimitar syndrome and distal tracheoesophageal fistula with esophageal atresia (type III b): a case report of diagnostic and therapeutic approach","authors":"Ida Nađ, Dorotea Šijak, A. Miculinić, D. Bartoniček, Maja Hrabak Paar, I. Malcic","doi":"10.1097/CP9.0000000000000042","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000042","url":null,"abstract":"Scimitar syndrome is a rare congenital heart defect (CHD) manifested by a partial abnormal inflow of pulmonary veins of the right lung into the suprahepatic segment of the inferior vena cava (VCI), making an angiographic image with the right heart edge similar to a Turkish saber (“scimitar”). It is found in only 1 to 3 per 100,000 births. Here we are presenting a patient who, in addition to the basic finding and presentation of a special partial anomalous inflow of pulmonary veins, also had other features of the Scimitar syndrome; dextroposition of the heart, without signs of heterotaxy, hypoplasia of the right lung, aberrant arterial supply of the right lung from the descending aorta (lung sequestration) with all hemodynamic signs of left-right flow (dilated right heart cavity and pulmonary artery), but without pulmonary hypertension. In addition, the patient had esophageal atresia with distal tracheoesophageal fistula (TEF). Treatment included operative occlusion of TEF with termino-terminal esophageal anastomosis. In the further course, esophagography revealed circular esophageal stenosis at the anastomosis site, but without the need for dilatation, which resolved spontaneously. Tracheotomy was needed due to the inability to separate from mechanical ventilation. Considering cardiopulmonary stability and the absence of pulmonary hypertension, a complete cardiosurgical correction was postponed to after the first year of life. The review is exceptional due to the concomitant occurrence of a TEF Vogt type IIIb, because the unusual combination of Scimitar syndrome with such type of TEF has not been described in the literature so far. To our knowledge, there is only one described case report with an H-type of TEF.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"63 - 66"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43660676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2023-01-01DOI: 10.1097/CP9.0000000000000039
Shanshan Gao, Song Gao, Zhen Sun, Mikael Åkesson, H. Shelat, Yongjian Geng
Background and purpose: Vascular smooth muscle cell (SMC) calcification represents a prominent phenotypic alteration in atherosclerosis. MicroRNA-322 (miR-322) is crucially involved in myogenic stem cell growth and differentiation. The galactosyltransferase 1-associated protein (GTAP) is a ubiquitin-conjugating enzyme E2Q1 (UBE2Q1) that serves as a critical mediator of post-translational regulation of certain cellular enzymes and transcription factors. Runt-related transcription factor 2 (Runx2) plays a critical role in arterial calcification. However, the interplay between miR-322, UBE2Q1, and Runx2 during cardiovascular calcification remain largely unknown. Therefore, the purpose of this study is to delineate the molecular mechanisms by which miR-322 regulates vascular calcification. Methods: Here we examined miR-322 expression in murine SMC, and determined whether miR-322 regulates SMC calcification via modulating expression of UBE2Q1 and calcifying proteins. Murine SMC cultures or aortic segments were exposed to inorganic phosphate (Pi) for induction of calcification. Expressions of calcification-related genes in SMC with lentivirus-mediated knockdown of UBE2Q1 were determined with Western blot analysis and quantitative real-time polymerase chain reaction (qRT-PCR). Luciferase reporter assay was performed to validate miR-322 target binding and SMC were transfected with anti-miR-322 oligonucleotides to inhibit miR-322 function. Results: Aortic rings derived from UBE2Q1−/− mice exhibited much higher calcium content compared to aortic rings from wildtype (WT) animals, following calcification induction. Knockdown of UBE2Q1 by lentiviral short hairpin RNA (shRNA) significantly enhanced the calcium deposition and expression of osteogenic gene Runx2 in SMC. Enhanced UBE2Q1 expression dramatically reduced calcification while promoting expression of contractile proteins SM22α and α-SMA. Treatment with anti-miR-322 diminished the luciferase activity in SMC transfected with the reporter gene driven by the 3′-untranslated region of UBE2Q1 mRNA. Anti-miR-322 treatment also inhibited calcification significantly. Conclusions: Our study identified miR-322 regulates vascular calcification by targeting UBE2Q1. The miR-322–dependent regulation of UBE2Q1 and calcification represents a novel regulatory mechanism that controls vascular SMC function during the pathogenesis of vascular calcification.
{"title":"MicroRNA-322 inhibition of calcification of arterial smooth muscle cells by regulation of galactosyltransferase 1-associating protein UBE2Q1 and Runx2","authors":"Shanshan Gao, Song Gao, Zhen Sun, Mikael Åkesson, H. Shelat, Yongjian Geng","doi":"10.1097/CP9.0000000000000039","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000039","url":null,"abstract":"Background and purpose: Vascular smooth muscle cell (SMC) calcification represents a prominent phenotypic alteration in atherosclerosis. MicroRNA-322 (miR-322) is crucially involved in myogenic stem cell growth and differentiation. The galactosyltransferase 1-associated protein (GTAP) is a ubiquitin-conjugating enzyme E2Q1 (UBE2Q1) that serves as a critical mediator of post-translational regulation of certain cellular enzymes and transcription factors. Runt-related transcription factor 2 (Runx2) plays a critical role in arterial calcification. However, the interplay between miR-322, UBE2Q1, and Runx2 during cardiovascular calcification remain largely unknown. Therefore, the purpose of this study is to delineate the molecular mechanisms by which miR-322 regulates vascular calcification. Methods: Here we examined miR-322 expression in murine SMC, and determined whether miR-322 regulates SMC calcification via modulating expression of UBE2Q1 and calcifying proteins. Murine SMC cultures or aortic segments were exposed to inorganic phosphate (Pi) for induction of calcification. Expressions of calcification-related genes in SMC with lentivirus-mediated knockdown of UBE2Q1 were determined with Western blot analysis and quantitative real-time polymerase chain reaction (qRT-PCR). Luciferase reporter assay was performed to validate miR-322 target binding and SMC were transfected with anti-miR-322 oligonucleotides to inhibit miR-322 function. Results: Aortic rings derived from UBE2Q1−/− mice exhibited much higher calcium content compared to aortic rings from wildtype (WT) animals, following calcification induction. Knockdown of UBE2Q1 by lentiviral short hairpin RNA (shRNA) significantly enhanced the calcium deposition and expression of osteogenic gene Runx2 in SMC. Enhanced UBE2Q1 expression dramatically reduced calcification while promoting expression of contractile proteins SM22α and α-SMA. Treatment with anti-miR-322 diminished the luciferase activity in SMC transfected with the reporter gene driven by the 3′-untranslated region of UBE2Q1 mRNA. Anti-miR-322 treatment also inhibited calcification significantly. Conclusions: Our study identified miR-322 regulates vascular calcification by targeting UBE2Q1. The miR-322–dependent regulation of UBE2Q1 and calcification represents a novel regulatory mechanism that controls vascular SMC function during the pathogenesis of vascular calcification.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"8 1","pages":"27 - 36"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46731118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-10-14DOI: 10.1097/cp9.0000000000000025
Dong Zhao
{"title":"Implications of updated epidemiological characteristics from heart diseases in China","authors":"Dong Zhao","doi":"10.1097/cp9.0000000000000025","DOIUrl":"https://doi.org/10.1097/cp9.0000000000000025","url":null,"abstract":"","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48919045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-10-11DOI: 10.1097/cp9.0000000000000024
Nanchao Hong, Wenzhi Pan, Daxin Zhou, J. Ge
{"title":"The China Heart Valve Center and National Transcatheter Valve Therapeutics Registry database","authors":"Nanchao Hong, Wenzhi Pan, Daxin Zhou, J. Ge","doi":"10.1097/cp9.0000000000000024","DOIUrl":"https://doi.org/10.1097/cp9.0000000000000024","url":null,"abstract":"","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43528266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Aortic dissection is a highly fatal disease with limited predictability requiring emergency response. It remains a challenging clinical problem and has a reported lower 5-year survival rate, especially in acute cases. Studying the epidemiology of aortic dissection can be important for targeting key populations and developing public health policies. Past studies have focused more on the in-hospital and follow-up mortality associated with aortic dissection but the global epidemiology review is still lacking. Incidence data have rarely been generated or provided. We estimated and analyzed the incidence of aortic dissection in all 195 countries and 54 regions worldwide and in the population structures of 15 selected countries. We further reviewed risk factors and baseline characteristics related to aortic dissection. We outlined the topic in terms of the biological, social, environmental, and psychosocial factors. Public health departments should screen target groups and key regions and introduce policies for disease prevention and relieve the high medical burdens.
{"title":"Aortic dissection: global epidemiology","authors":"Jianhan Yin, Feng Liu, Jiabin Wang, P. Yuan, Shuangjing Wang, Wei Guo","doi":"10.1097/CP9.0000000000000028","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000028","url":null,"abstract":"Aortic dissection is a highly fatal disease with limited predictability requiring emergency response. It remains a challenging clinical problem and has a reported lower 5-year survival rate, especially in acute cases. Studying the epidemiology of aortic dissection can be important for targeting key populations and developing public health policies. Past studies have focused more on the in-hospital and follow-up mortality associated with aortic dissection but the global epidemiology review is still lacking. Incidence data have rarely been generated or provided. We estimated and analyzed the incidence of aortic dissection in all 195 countries and 54 regions worldwide and in the population structures of 15 selected countries. We further reviewed risk factors and baseline characteristics related to aortic dissection. We outlined the topic in terms of the biological, social, environmental, and psychosocial factors. Public health departments should screen target groups and key regions and introduce policies for disease prevention and relieve the high medical burdens.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"151 - 161"},"PeriodicalIF":0.0,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42802408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-10-01DOI: 10.1097/CP9.0000000000000030
S. Sundari, Mansour S Alturki, Ian Steinke, J. Deruiter, S. Ramesh, Manoj Govindarajulu, M. Almaghrabi, Suhrud Pathak, A. M. Rassa, K. M. Shafeeq, Payton Lowery, Rishi M. Nadar, R. Babu, Jun Ren, K. Rani, Forrest Smith, Timothy Moore, M. Dhanasekaran
Background and purpose: Medication-induced cardiotoxicity is a significant factor in the attrition of drugs during preclinical and clinical development processes. Patients with diabetes mellitus (hyperglycemic) are more than twice as likely to experience cardiac failure. Additionally, type 2 diabetes mellitus (T2D) patients often display significant hyperarousal-related clinical anomalies such as fear, panic, nervousness, pain, and seizures. Consequently, hyperarousal in patients with inadequate metabolic outcomes (hyperglycemic conditions) is usually treated with drugs that block sodium/calcium channels, augment inhibitory (gamma-aminobutyric acid [GABA]) neurotransmission, and reduce excitatory (glutamatergic) neurotransmission. These perilous combined clinical-pathological conditions of hyperglycemia and hypoarousal may result in severe learning disabilities and cognitive impairment. Unfortunately, only a few studies have investigated the synergistic effects of hypoarousal and hyperglycemia on cognition. Methods: General behavioral assessment, plus maze, Y-maze spontaneous alternation, Hebb-Williams maze and Passive avoidance paradigm were evaluated in this study. The current study assessed the in silico structural properties attributed to its pharmacodynamic actions and interaction with Gamma-aminobutyric acid (GABA) and insulin receptors using Schrodinger and LigPrep software. Results: The administration of alloxan and phenytoin induced significant learning and cognitive deficiencies. Based on the in silico studies, alloxan is a better drug to induce hyperglycemia as compared to the well-established hyperglycemic agent, streptozotocin (STZ). Conclusions: The current study indicated that administering alloxan and phenytoin to rodents can serve as a valid animal model to understand the pathophysiology associated with hypoarousal and hyperglycemia-mediated cognitive impairment and to identify novel therapeutic interventions for hyperglycemic and hypoarousal-related learning and cognitive deficiency.
{"title":"Cardiovascular toxin-induced hyperglycemic and hypoarousal pathology-associated cognitive impairment: an in silico and in vivo validation","authors":"S. Sundari, Mansour S Alturki, Ian Steinke, J. Deruiter, S. Ramesh, Manoj Govindarajulu, M. Almaghrabi, Suhrud Pathak, A. M. Rassa, K. M. Shafeeq, Payton Lowery, Rishi M. Nadar, R. Babu, Jun Ren, K. Rani, Forrest Smith, Timothy Moore, M. Dhanasekaran","doi":"10.1097/CP9.0000000000000030","DOIUrl":"https://doi.org/10.1097/CP9.0000000000000030","url":null,"abstract":"Background and purpose: Medication-induced cardiotoxicity is a significant factor in the attrition of drugs during preclinical and clinical development processes. Patients with diabetes mellitus (hyperglycemic) are more than twice as likely to experience cardiac failure. Additionally, type 2 diabetes mellitus (T2D) patients often display significant hyperarousal-related clinical anomalies such as fear, panic, nervousness, pain, and seizures. Consequently, hyperarousal in patients with inadequate metabolic outcomes (hyperglycemic conditions) is usually treated with drugs that block sodium/calcium channels, augment inhibitory (gamma-aminobutyric acid [GABA]) neurotransmission, and reduce excitatory (glutamatergic) neurotransmission. These perilous combined clinical-pathological conditions of hyperglycemia and hypoarousal may result in severe learning disabilities and cognitive impairment. Unfortunately, only a few studies have investigated the synergistic effects of hypoarousal and hyperglycemia on cognition. Methods: General behavioral assessment, plus maze, Y-maze spontaneous alternation, Hebb-Williams maze and Passive avoidance paradigm were evaluated in this study. The current study assessed the in silico structural properties attributed to its pharmacodynamic actions and interaction with Gamma-aminobutyric acid (GABA) and insulin receptors using Schrodinger and LigPrep software. Results: The administration of alloxan and phenytoin induced significant learning and cognitive deficiencies. Based on the in silico studies, alloxan is a better drug to induce hyperglycemia as compared to the well-established hyperglycemic agent, streptozotocin (STZ). Conclusions: The current study indicated that administering alloxan and phenytoin to rodents can serve as a valid animal model to understand the pathophysiology associated with hypoarousal and hyperglycemia-mediated cognitive impairment and to identify novel therapeutic interventions for hyperglycemic and hypoarousal-related learning and cognitive deficiency.","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":"7 1","pages":"178 - 185"},"PeriodicalIF":0.0,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41904653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-10-01DOI: 10.1097/cp9.0000000000000029
X. Chu, B. Feng, J. Ge, Lixin Guo, Y. Huo, L. Ji, Qian Jia, Song Jiang, Yong Li, Fang Liu, Xinfeng Liu, Yuping Liu, Bin Lu, Ankang Lv, Yongjun Wang, J. Weng, Qiang Zeng, Yingmei Zhang, Jingmin Zhou
{"title":"Chinese expert consensus on the risk assessment and management of panvascular disease inpatients with type 2 diabetes mellitus (2022 edition)","authors":"X. Chu, B. Feng, J. Ge, Lixin Guo, Y. Huo, L. Ji, Qian Jia, Song Jiang, Yong Li, Fang Liu, Xinfeng Liu, Yuping Liu, Bin Lu, Ankang Lv, Yongjun Wang, J. Weng, Qiang Zeng, Yingmei Zhang, Jingmin Zhou","doi":"10.1097/cp9.0000000000000029","DOIUrl":"https://doi.org/10.1097/cp9.0000000000000029","url":null,"abstract":"","PeriodicalId":52908,"journal":{"name":"Cardiology Plus","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47524113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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