Journal of molecular and cellular cardiology plus最新文献

{"title":"Targeting the CD39/CD73 pathway: New insights into cardiac fibrosis and inflammation in female cardiac surgery patients","authors":"Eitezaz Mahmood ,&nbsp;Mark Robitaille ,&nbsp;Yifan Bu ,&nbsp;Adnan Khan ,&nbsp;Marie-France Poulin ,&nbsp;Feroze Mahmood ,&nbsp;Ruma Bose ,&nbsp;Kamal R. Khabbaz ,&nbsp;Simon C. Robson ,&nbsp;Robina Matyal","doi":"10.1016/j.jmccpl.2025.100294","DOIUrl":"10.1016/j.jmccpl.2025.100294","url":null,"abstract":"<div><div>Women undergoing cardiac surgery suffer from worse outcomes than their male counterparts. The reasons for this disparity are multifactorial, but the loss of the protective effects of estrogen likely plays a role. Estrogen acts on the CD39/CD73 purine pathway, and loss of estrogen effects may contribute to the increased inflammation seen in post-menopausal women. We aimed to compare CD39/CD73 expression and downstream fibrosis, and inflammation in men and women undergoing cardiac surgery and then used an ovariectomy/high fat diet mouse model to approximate women who present for cardiac surgery to test therapeutics. We found decreased CD39 and CD73 in women compared to men, which was associated with increased fibrosis. Apyrase supplementation (a CD39 mimetic) improved ejection fraction and decreased E/e’. Increased CD73 function (via dipyridamole) decreased fibrosis. This study demonstrates the importance of purinergic dysfunction in cardiovascular disease in women and presents two potential therapeutics to improve cardiac health via manipulation of purine pathways.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"12 ","pages":"Article 100294"},"PeriodicalIF":0.0,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143726112","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}

{"title":"Electrophysiological comparison of left versus right stellate ganglia neurons","authors":"Arie O. Verkerk ,&nbsp;Carol Ann Remme ,&nbsp;Molly O'Reilly","doi":"10.1016/j.jmccpl.2025.100293","DOIUrl":"10.1016/j.jmccpl.2025.100293","url":null,"abstract":"<div><h3>Background</h3><div>The stellate ganglia of the peripheral autonomic nervous system innervate the heart and continuously fine-tune cardiac function to meet physiological demands. The right stellate ganglion (RSG) predominantly innervates the sinoatrial node and has functional effects on chronotropy/heart rate, whereas the left stellate ganglion (LSG) has predominance in the ventricular myocardium and impacts inotropy/contractility. Whilst the innervation patterns and functional consequences of block and stimulation are well-documented, basic electrophysiological characterisation and single-cell comparison of RSG and LSG neurons has not been performed. In addition, sex differences in stellate ganglion action potential (AP) parameters may exist, but remain as yet unknown.</div></div><div><h3>Methods/results</h3><div>Here we characterise the electrical properties of enzymatically isolated mouse stellate ganglia neurons using the patch clamp technique. Using 500 ms depolarising pulses of varying amplitude, we provide detailed characterisation of basic AP properties and their correlations. We reveal that there are two populations of neurons in terms of their AP firing properties (phasic or tonic firing), with the majority (65 %) firing with a phasic pattern. When all recordings were pooled, tonic neurons had a significantly larger AP amplitude (85 ± 3.0 vs 76 ± 2.4 mV) and overshoot (28 ± 1.8 vs 19 ± 1.8 mV) compared to phasic neurons (<em>P</em> &lt; 0.05). Moreover, phasic neurons did not fire spontaneously, whereas 50 % of tonic neurons did, and more often presented with anodal break excitation (<em>P</em> &lt; 0.05). When male vs female neurons were compared (with LSG and RSG neurons as subgroups), males had a more negative minimum diastolic potential (MDP; −55 ± 1.7 vs −47 ± 3.0 mV, <em>P</em> &lt; 0.05) and higher percentage of anodal break excitation (<em>P</em> ≤ 0.05). When LSG vs RSG neurons were compared (with gender as subgroups), no significant differences were observed except a higher percentage of anodal break excitation in the RSG (<em>P</em> ≤ 0.05).</div></div><div><h3>Conclusions</h3><div>Isolated RSG and LSG neurons have similar AP firing patterns and properties. A significant difference was observed in the MDP and anodal break excitation of male vs female neurons. However, all other AP parameters were similar. This suggests that the LSG and RSG can be combined irrespective of sex when investigating the electrophysiological properties of these distinct anatomical structures.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"12 ","pages":"Article 100293"},"PeriodicalIF":0.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143696710","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}

{"title":"Gemfibrozil mitigates caspase-11-driven myocardial pyroptosis in ischemia/reperfusion injury in mice","authors":"Tetsuro Marunouchi,&nbsp;Mayu Kyono,&nbsp;Naoko Kikuchi,&nbsp;Kouichi Tanonaka","doi":"10.1016/j.jmccpl.2025.100292","DOIUrl":"10.1016/j.jmccpl.2025.100292","url":null,"abstract":"<div><div>The size of the infarct area following acute myocardial infarction (AMI) is a critical prognostic factor. Caspase-11-dependent pyroptosis has been implicated as a key mechanism driving cardiomyocyte death after AMI. However, no therapeutic agents have been developed to inhibit myocardial cell death by targeting caspase-11. This study investigates the effects of gemfibrozil, a potential caspase-11 inhibitor, on ischemia/reperfusion-induced myocardial pyroptosis in mice. To model AMI, the left coronary artery of C57BL/6 N mice was ligated for 1 h, followed by reperfusion. Levels of cleaved caspase-11 and the N-terminal fragment of gasdermin D (GSDMD-N) in ischemic myocardial tissue increased progressively over time after ischemia/reperfusion. Gemfibrozil treatment during reperfusion significantly attenuated these increases in cleaved caspase-11 and GSDMD-N levels. Moreover, gemfibrozil reduced the extent of myocardial infarct size during reperfusion. In cultured cardiomyocytes isolated from adult mice, hypoxia/reoxygenation-induced increases in caspase-11 and GSDMD cleavage were similarly mitigated by gemfibrozil, which concurrently prevented necrotic cell death. These findings demonstrate the involvement of caspase-11-dependent pyroptosis in myocardial cell death following ischemia/reperfusion and suggest that gemfibrozil holds promise as a therapeutic agent for reducing myocardial infarct size after AMI.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"12 ","pages":"Article 100292"},"PeriodicalIF":0.0,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143591718","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}

{"title":"Innovations in heart failure management: The role of cutting-edge biomarkers and multi-omics integration","authors":"Jose Mesquita Bastos ,&nbsp;Beatriz Colaço ,&nbsp;Rui Baptista ,&nbsp;Cristina Gavina ,&nbsp;Rui Vitorino","doi":"10.1016/j.jmccpl.2025.100290","DOIUrl":"10.1016/j.jmccpl.2025.100290","url":null,"abstract":"<div><div>Heart failure (HF) remains a major cause of morbidity and mortality worldwide and represents a major challenge for diagnosis, prognosis and treatment due to its heterogeneity. Traditional biomarkers such as BNP and NT-proBNP are valuable but insufficient to capture the complexity of HF, especially phenotypes such as HF with preserved ejection fraction (HFpEF). Recent advances in multi-omics technology and novel biomarkers such as cell-free DNA (cfDNA), microRNAs (miRNAs), ST2 and galectin-3 offer transformative potential for HF management. This review explores the integration of these innovative biomarkers into clinical practice and highlights their benefits, such as improved diagnostic accuracy, enhanced risk stratification and non-invasive monitoring capabilities. By leveraging multi-omics approaches, including lipidomics and metabolomics, clinicians can uncover new pathways, refine the classification of HF phenotypes, and develop personalized therapeutic strategies tailored to individual patient profiles. Remarkable advances in proteomics and metabolomics have identified biomarkers associated with key HF mechanisms such as mitochondrial dysfunction, inflammation and fibrosis, paving the way for targeted therapies and early interventions. Despite the promising results, significant challenges remain in translating these findings into routine care, including high costs, technical limitations and the need for large-scale validation studies. This report argues for an integrative, multi-omics-based model to overcome these obstacles and emphasizes the importance of collaboration between researchers, clinicians and policy makers. By linking innovative science with practical applications, multi-omics approaches have the potential to redefine HF management and lead to better patient outcomes and more sustainable healthcare systems.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"11 ","pages":"Article 100290"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143570526","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}

{"title":"ADAMTS7, a target in atherosclerosis, cooperates with its homolog ADAMTS12 to protect against myxomatous valve degeneration","authors":"Timothy J. Mead ,&nbsp;Sumit Bhutada ,&nbsp;Niccolò Peruzzi ,&nbsp;Janet Adegboye ,&nbsp;Deborah E. Seifert ,&nbsp;Elisabeth Cahill ,&nbsp;Jeanne Drinko ,&nbsp;Eoin Donnellan ,&nbsp;Anu Guggiliam ,&nbsp;Zoran Popovic ,&nbsp;Brian Griffin ,&nbsp;Karin Tran-Lundmark ,&nbsp;Suneel S. Apte","doi":"10.1016/j.jmccpl.2025.100288","DOIUrl":"10.1016/j.jmccpl.2025.100288","url":null,"abstract":"<div><div>The physiological roles of the metalloprotease-proteoglycan ADAMTS7, a drug target in atherosclerosis and vascular restenosis, and its homolog ADAMTS12, are undefined in the cardiovascular system. The objective of the present work was to investigate their roles in mice with genetic inactivation of both proteases and in relation to the resulting valve defects, to define their proteolytic activities in the matrisome. Here, we demonstrate that <em>Adamts7</em> and <em>Adamts12</em> are co-expressed in heart valves and each buffers inactivation of the other by compensatory upregulation. Leaflets of <em>Adamts7</em>^−/−;<em>Adamts12</em>^−/− aortic valves, but not the respective single mutants, were abnormally shaped at birth, with progressively severe disorganization and enlargement occurring thereafter. Doppler echocardiography showed that <em>Adamts7</em>^−/−;<em>Adamts12</em>^−/− mice had stenotic and regurgitant aortic valves. We investigated ADAMTS7 and ADAMTS12 substrates relevant to the valve matrisome in secretome libraries from <em>Adamts7</em>^−/−;<em>Adamts12</em>^−/− cells using the N-terminomics technique Terminal Amine Isotopic Labeling of Substrates (TAILS). Although ADAMTS7 and ADAMTS12 shared several extracellular matrix (ECM) substrates, cleavage sites and sequence preference for each protease were distinct. <em>Adamts7</em>^−/−;<em>Adamts12</em>^−/− valve leaflets showed accumulation of several of the identified ECM substrates, including periostin, a matricellular protein crucial for cardiac valve homeostasis. We conclude that the myxomatous degeneration in <em>Adamts7</em>^−/−;<em>Adamts12</em>^−/− valve leaflets reflects a complex disturbance of ECM proteostasis with accumulation of multiple ADAMTS7 and ADAMTS12 ECM substrates, and perturbation of regulatory pathways with roots in ECM, such as TGFβ signaling, which was increased in the mutant valves.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"11 ","pages":"Article 100288"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143529374","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}

{"title":"IFNγ activates an immune-like regulatory network in the cardiac vascular endothelium","authors":"Timothy D. Arthur ,&nbsp;Isaac N. Joshua ,&nbsp;Jennifer P. Nguyen ,&nbsp;Agnieszka D'Antonio-Chronowska ,&nbsp;Matteo D'Antonio ,&nbsp;Kelly A. Frazer","doi":"10.1016/j.jmccpl.2025.100289","DOIUrl":"10.1016/j.jmccpl.2025.100289","url":null,"abstract":"<div><div>The regulatory mechanisms underlying the response to pro-inflammatory cytokines in cardiac diseases are poorly understood. Here, we use iPSC-derived cardiovascular progenitor cells (CVPCs) to model the response to interferon gamma (IFNγ) in human cardiac tissue. We generate RNA-seq and ATAC-seq for four CVPCs that were treated with IFNγ and compare them with paired untreated controls. Transcriptional differences after treatment show that IFNγ initiates an innate immune cell-like response, shifts the CVPC transcriptome toward coronary artery and aorta profiles, and stimulates expression of endothelial cell-specific genes. Analysis of the accessible chromatin shows that IFNγ is a potent chromatin remodeler and establishes an IRF-STAT immune-cell like regulatory network. Finally, we show that 11 GWAS risk variants for 8 common cardiac diseases overlap IFNγ-upregulated ATAC-seq peaks. Our findings reveal insights into IFNγ-induced activation of an immune-like regulatory network in human cardiac tissue and the potential role that regulatory elements in this pathway play in common cardiac diseases.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"11 ","pages":"Article 100289"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143527368","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}

{"title":"Loss of Snord116 protects cardiomyocyte kinetics during ischemic stress","authors":"Lucy E. Pilcher ,&nbsp;Emmaleigh Hancock ,&nbsp;Akshay Neeli ,&nbsp;Maria Sckolnick ,&nbsp;Matthew A. Caporizzo ,&nbsp;Bradley M. Palmer ,&nbsp;Jeffrey L. Spees","doi":"10.1016/j.jmccpl.2025.100291","DOIUrl":"10.1016/j.jmccpl.2025.100291","url":null,"abstract":"<div><div>Loss of Snord116, a non-coding RNA, causes Prader Willi Syndrome (PWS), a complex disorder with circadian, metabolic, neurologic, and cardiovascular phenotypes. The Snord116 paternal knockout (Snord116p-) mouse, a model of PWS, demonstrated differential methylation of thousands of genes involved in regulation of metabolism, epigenetics, and ion homeostasis. To determine if Snord116 expression influences the cardiomyocyte response to acute ischemia, we developed a model of ischemia and reperfusion using living myocardial slices and monitored cardiomyocyte function in slices derived from Snord116p- mice and wildtype littermates (WT LM) of both sexes. We found that Snord116 loss reduced ischemia-induced systolic prolongation and delayed diastolic elongation in slices from both males and females. Furthermore, when compared with slices from males, slices from females experienced a greater increase in end-diastolic force after ischemia. We conclude that female myocardium responds more dramatically and quickly to ischemic injury in this model and that loss of Snord116 is cardioprotective; this allows for a more complete myocardial recovery following reperfusion.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"11 ","pages":"Article 100291"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143552305","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}

{"title":"Angiotensin IV does not exert prothrombotic effects in vivo","authors":"Qifang Wu ,&nbsp;Christine Gille ,&nbsp;Florian Maderspacher ,&nbsp;Bianca Hildebrand ,&nbsp;Manuela Thienel ,&nbsp;Sebastian Clauss","doi":"10.1016/j.jmccpl.2025.100287","DOIUrl":"10.1016/j.jmccpl.2025.100287","url":null,"abstract":"<div><div>Thrombosis and thromboembolism are serious clinical complications of cardiovascular diseases and are among the leading causes of mortality worldwide. Dysregulation of the renin-angiotensin system is associated with an increased incidence of thrombotic events. Angiotensin II (AngII) is known to enhance platelet aggregation, contributing to a prothrombotic state in patients. Important biological roles of other angiotensin peptides and their receptors have been shown, but their specific role in thrombus formation remains unclear. Recent evidence suggests a prothrombotic role of angiotensin IV (AngIV). To confirm the prothrombotic effects of AngIV and to further investigate AngIV-mediated mechanisms, we utilized osmotic minipumps to administer AngIV in mice continuously over 4 weeks. AngIV treatment did not induce thrombus formation in the heart, did not affect platelet numbers, and did not enhance platelet aggregation. HGF, c-MET, or PAI-1 expression levels in the heart were not affected by AngIV treatment in mice. Furthermore, we did not observe altered platelet aggregation of human platelets incubated with HGF. These findings indicate that AngIV does not regulate key prothrombotic mechanisms.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"11 ","pages":"Article 100287"},"PeriodicalIF":0.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143421256","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}

{"title":"In-depth proteomic profiling identifies potentiation of the LPS response by 7-ketocholesterol","authors":"Iain R. Phair ,&nbsp;Magdalena Sovakova ,&nbsp;Noor Alqurashi ,&nbsp;Raid B. Nisr ,&nbsp;Alison D. McNeilly ,&nbsp;Douglas Lamont ,&nbsp;Graham Rena","doi":"10.1016/j.jmccpl.2025.100285","DOIUrl":"10.1016/j.jmccpl.2025.100285","url":null,"abstract":"<div><div>In patients with stable coronary artery disease, plasma levels of 7-ketocholesterol (7-KC), found at high levels in atherosclerotic lesions, predict risk of incident heart failure dose dependently, potentially contributing to disease aetiology. Previous studies demonstrated that 7-KC can elicit effects on macrophage function; however, effects of 7-KC on the macrophage proteome have not been studied systematically. Here we used quantitative mass spectrometry to establish the effect of 7-KC on the mouse macrophage proteome. 7-KC independently mediated dynamic changes, including on atherogenic/M1 markers, cholesterol metabolism, biosynthesis and transport, as well as nutrient transport more broadly. These changes were however insufficient alone to drive changes in cytokine and chemokine secretion. Rather, they prime the macrophage, potentiating LPS-stimulated TNF alpha secretion and key pro-inflammatory enzymes. Our results indicate that 7-KC has independent metabolic effects on the macrophage; however, effects on the immune system are primarily due to the changes in metabolism priming the response to an inflammatory stimulus. Earlier findings from CANTOS and the recent FDA approval of colchicine highlight that inflammation is a viable target for cardiovascular disease; however, it is currrently unclear which will be the best anti-inflammatory targets to pursue in the future. In this context, our findings suggest that drugs targeting atherogenic markers induced by 7-KC might be well tolerated, as they will not necessarily be expected to be immunosuppressive.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"11 ","pages":"Article 100285"},"PeriodicalIF":0.0,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143164833","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}

{"title":"Circulating levels of miR-20b-5p are associated with survival in cardiogenic shock","authors":"Tuomas Mäntylä ,&nbsp;Chunguang Wang ,&nbsp;Mikko Hänninen ,&nbsp;Katariina Immonen ,&nbsp;Toni Jäntti ,&nbsp;Johan Lassus ,&nbsp;Ilkka Tikkanen ,&nbsp;Kari Pulkki ,&nbsp;Yvan Devaux ,&nbsp;Veli-Pekka Harjola ,&nbsp;Päivi Lakkisto ,&nbsp;CardShock Study Investigators","doi":"10.1016/j.jmccpl.2025.100284","DOIUrl":"10.1016/j.jmccpl.2025.100284","url":null,"abstract":"<div><div>Cardiogenic shock (CS) is a medical emergency with high in-hospital mortality. New biomarkers are needed to identify patients at a greater risk of adverse outcomes. This study aimed to investigate the prognostic potential of microRNAs (miRNAs) in assessment of the outcome of cardiogenic shock.</div><div>Circulating miRNA levels were measured by quantitative PCR in plasma samples collected at baseline from 165 patients of the multicenter, prospective, observational CardShock study and compared between in-hospital and 90-day survivors and non-survivors. Of the 10 studied miRNAs, median levels of miR-20b-5p at baseline were significantly higher in in-hospital and 90-day survivors compared to non-survivors [median 0.014 arbitrary units (AU) (interquartile range (IQR) 0.003–0.024) <em>vs.</em> 0.008 AU (IQR 0.001–0.015), <em>p</em> = 0.013] and [0.015 AU (IQR 0.003–0.025) <em>vs.</em> 0.010 AU (IQR 0.001–0.015), <em>p</em> = 0.012], respectively. In Cox regression analysis, miR-20b-5p levels in the highest quartile were significantly associated with 90-day survival (adjusted hazard ratio 2.47 (95 % confidence interval 1.16–5.28), <em>p</em> = 0.019) when adjusted for CardShock Risk Score variables (age, confusion at presentation, previous myocardial infarction or coronary artery bypass grafting, acute coronary syndrome (ACS) etiology, left ventricular ejection fraction, lactate, and estimated glomerular filtration rate). A similar association of highest quartile miR-20b-5p levels with 90-day survival was also confirmed in ACS patient subcohort (79 % of CS patients).</div><div>The results of this study indicate that circulating levels of miR-20b-5p at baseline could help in assessing in-hospital and 90-day survival in CS patients.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"11 ","pages":"Article 100284"},"PeriodicalIF":0.0,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143164832","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}