Journal of molecular and cellular cardiology plus最新文献

{"title":"Diet reversal improves hyperglycaemia-related coronary dysfunction and attenuates subsequent myocardial ischemia/reperfusion injury.","authors":"Juma El-Awaisi , Simon Cleary , Dean Kavanagh , David Hodson , Neena Kalia","doi":"10.1016/j.jmccpl.2024.100100","DOIUrl":"10.1016/j.jmccpl.2024.100100","url":null,"abstract":"","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"10 ","pages":"Article 100100"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142747101","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":"Increased Atrial Fibrillation burden in Heart Failure is associated with increased vulnerability to atrial alternans","authors":"George Madders , Alice Whitley, Mohammed Obeidat, Menglu Li, Agnieszka Swiderskwa, Charlotte Smith, David Eisner, Andrew Trafford, Katharine Dibb","doi":"10.1016/j.jmccpl.2024.100105","DOIUrl":"10.1016/j.jmccpl.2024.100105","url":null,"abstract":"","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"10 ","pages":"Article 100105"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142743427","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":"Role of peroxisomes in compensatory metabolic adaptation in Barth syndrome Cardiomyopathy","authors":"Elsie Vidah Kajese , Malte Hachmann , Christoph Maack , Srikanth Karnati , Jan Dudek","doi":"10.1016/j.jmccpl.2024.100113","DOIUrl":"10.1016/j.jmccpl.2024.100113","url":null,"abstract":"","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"10 ","pages":"Article 100113"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142744815","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":"The SGLT2 inhibitor empagliflozin directly increases ketone utilisation in ischaemic hearts independent of substrate supply","authors":"Dylan Chase , Thomas R. Eykyn , Michael J. Shattock , Yu Jin Chung","doi":"10.1016/j.jmccpl.2024.100117","DOIUrl":"10.1016/j.jmccpl.2024.100117","url":null,"abstract":"","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"10 ","pages":"Article 100117"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142745402","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":"ATRIAL FIBRILLATION INDUCIBILITY IS HIGHER IN STRENUOUS EXERCISE DUE TO AN INCREASE IN FIBROSIS AND LOCAL INFLAMMATION IN A TRAINED ANIMAL MODEL","authors":"Anna Alcarraz , Aline Meza-Ramos , Cira Rubies , Maria Sanz- De La Garza , Lluis Mont , Montserrat Batlle , Eduard Guasch","doi":"10.1016/j.jmccpl.2024.100096","DOIUrl":"10.1016/j.jmccpl.2024.100096","url":null,"abstract":"","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"10 ","pages":"Article 100096"},"PeriodicalIF":0.0,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142747695","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":"Nitazene opioids and the heart: Identification of a cardiac ion channel target for illicit nitazene opioids","authors":"Jules C. Hancox ,&nbsp;Yibo Wang ,&nbsp;Caroline S. Copeland ,&nbsp;Henggui Zhang ,&nbsp;Stephen C. Harmer ,&nbsp;Graeme Henderson","doi":"10.1016/j.jmccpl.2024.100118","DOIUrl":"10.1016/j.jmccpl.2024.100118","url":null,"abstract":"<div><div>The growing use of nitazene synthetic opioids heralds a new phase of the opioid crisis. However, limited information exists on the toxic effects of these drugs, aside from a propensity for respiratory depression. With restricted research availability of nitazenes, we used machine-learning-based tools to evaluate five nitazene compounds' interaction potential with the hERG potassium channel, a key drug antitarget in the heart. All nitazenes were predicted to inhibit hERG with low μM IC₅₀ values. These findings indicate a potential for proarrhythmic hERG block by nitazene opioids, warranting detailed cardiac safety evaluations of these drugs.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"10 ","pages":"Article 100118"},"PeriodicalIF":0.0,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142553209","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":"Transcriptome analysis of the aortic coarctation area","authors":"Rada Ellegård ,&nbsp;Torsten Malm ,&nbsp;Constance G. Weismann ,&nbsp;Eva Fernlund ,&nbsp;Swedish National Biobank for Congenital Heart Disease (SNAB-CHD) consortium,&nbsp;Anneli Nordén Björnlert ,&nbsp;Hanna Klang Årstrand ,&nbsp;Katarina Ellnebo-Svedlund ,&nbsp;Cecilia Gunnarsson","doi":"10.1016/j.jmccpl.2024.100094","DOIUrl":"10.1016/j.jmccpl.2024.100094","url":null,"abstract":"<div><h3>Background</h3><div>Coarctation of the aorta (CoA) is a relatively common congenital heart defect. The underlying causes are not known, but a combination of genetic factors and abnormalities linked to embryonic development is suspected. There are only a few studies of the underlying molecular mechanisms in CoA. The aim of the current study was to expand our understanding of the pathogenesis of CoA by characterizing the transcriptome of the coarctation area.</div></div><div><h3>Methods</h3><div>Tissue samples from 21 pediatric patients operated for CoA were dissected into separate biopsies consisting of the localized coarctation itself, proximal/distal tissue and ductus. RNA was sequenced to evaluate gene expression in the different biopsies.</div></div><div><h3>Results</h3><div>We observed an activation of acute phase response in samples from the localized coarctation compared to samples from distal or proximal tissue. However, we observed even bigger differences for patient age and sex than compared to biopsy location. A cluster of genes located at 1q21, including the S100 gene family, displayed contrasting expression depending on patient sex, and appeared to affect the balance between inflammatory and interferon pathways. Biopsies from patients &lt;3 months old were characterized by a significantly higher fibrotic activity compared to samples from older patients. The ductus tissue was characterized by an upregulation of factors associated with proliferation.</div></div><div><h3>Conclusions</h3><div>The ongoing processes in the coarctation area are influenced by the age and sex of the patient, and possibly by differences in etiology between different patients. The impact of patient attributes must be taken into consideration when performing future studies.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"10 ","pages":"Article 100094"},"PeriodicalIF":0.0,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772976124000345/pdfft?md5=c075465d71ff736e6bcc8d95cc7ac49d&pid=1-s2.0-S2772976124000345-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142315871","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":"Conditional ablation of MCU exacerbated cardiac pathology in a genetic arrhythmic model of CPVT","authors":"Arpita Deb ,&nbsp;Brian D. Tow ,&nbsp;Jie Hao ,&nbsp;Branden L. Nguyen ,&nbsp;Valeria Gomez ,&nbsp;James A. Stewart Jr ,&nbsp;Ashley J. Smuder ,&nbsp;Bjorn C. Knollmann ,&nbsp;Ying Wang ,&nbsp;Bin Liu","doi":"10.1016/j.jmccpl.2024.100093","DOIUrl":"10.1016/j.jmccpl.2024.100093","url":null,"abstract":"<div><h3>Background</h3><p>Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a genetic arrhythmic syndrome caused by mutations in the calcium (Ca²⁺) release channel ryanodine receptor (RyR2) and its accessory proteins. These mutations make the channel leaky, resulting in Ca²⁺-dependent arrhythmias. Besides arrhythmias, CPVT hearts typically lack structural cardiac remodeling, a characteristic often observed in other cardiac conditions (heart failure, prediabetes) also marked by RyR2 leak. Recent studies suggest that mitochondria are able to accommodate more Ca²⁺ influx to inhibit arrhythmias in CPVT. Thus, we hypothesize that CPVT mitochondria can absorb diastolic Ca²⁺ to protect the heart from cardiac remodeling.</p></div><div><h3>Methods and results</h3><p>The Mitochondrial Ca²⁺ uniporter (MCU), the main mitochondrial Ca²⁺ uptake protein, was conditionally knocked out in a CPVT model of calsequestrin 2 (CASQ2) KO. In vivo cardiac function was impaired in the CASQ2^−/−-MCU^CKO model as assessed by echocardiography. Cardiac dilation and cellular hypertrophy were also observed in the CASQ2^−/−-MCU^CKO hearts. Live-cell imaging identified altered Ca²⁺ handling and increased oxidative stress in CASQ2^−/−-MCU^CKO myocytes. The activation status of Ca²⁺-dependent remodeling pathways (CaMKII, Calcineurin) was not altered in the CASQ2^−/−-MCU^CKO model. RNAseq identified changes in the transcriptome of the CASQ2^−/−-MCU^CKO hearts, distinct from the classic cardiac remodeling program of fetal gene re-expression.</p></div><div><h3>Conclusions</h3><p>We present genetic evidence that mitochondria play a protective role in CPVT. MCU-dependent Ca²⁺ uptake is crucial for preventing pathological cardiac remodeling in CPVT.</p></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"10 ","pages":"Article 100093"},"PeriodicalIF":0.0,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772976124000333/pdfft?md5=8ef6c8a61076f2dcb4155d45ed6349eb&pid=1-s2.0-S2772976124000333-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142233710","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":"P-, E-, and H-cadherins differ in their relationships with coronary stenosis, cardiovascular outcomes, and unplanned recurrent revascularization","authors":"Nadezhda G. Gumanova ,&nbsp;Dmitry K. Vasilyev ,&nbsp;Natalya L. Bogdanova ,&nbsp;Yaroslav I. Havrichenko ,&nbsp;Oxana M. Drapkina","doi":"10.1016/j.jmccpl.2024.100091","DOIUrl":"10.1016/j.jmccpl.2024.100091","url":null,"abstract":"<div><h3>Background and aims</h3><p>Cadherins are adhesion proteins, and their dysregulation may result in the development of atherosclerosis, plaque rupture, or lesions of the vascular wall. The aim of the present study was to detect the associations of cadherins-P, −E, and <img>H, with atherosclerosis and pathological cardiovascular conditions.</p></div><div><h3>Methods and results</h3><p>The present study with 3-year follow up evaluated atherosclerosis and fasting levels of P-, E-, and H-cadherins in the serum samples of 214 patients in a hospital setting. Coronary lesions were assessed by coronary angiography as Gensini score. Serum proteomic profiling was performed using antibody microarrays. The contents of P-, E-, and H-cadherins in the serum were measured using indirect ELISA. High levels of P- and E-cadherins and low levels of H-cadherin were associated with severity of atherosclerosis. High levels of P- and E-cadherins were associated with higher incidence of nonfatal cardiovascular outcomes. E-cadherin was associated with higher incidence of recurrent revascularization during 3 year follow-up. The results of Spearman rank correlation analysis revealed various associations of the three cadherins with lipid, endothelial, and metabolic biomarkers.</p></div><div><h3>Conclusions</h3><p>The data indicated that classical and atypical cadherins were associated with atherosclerosis progression. Elevated levels of P-cadherin were associated with coronary atherosclerosis. The data indicated that various lipid, endothelial, and metabolic biomarkers may influence the levels of cadherins. Thus, P-, E-, and H-cadherins may be promising markers for the assessment of cardiovascular risk.</p></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"9 ","pages":"Article 100091"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S277297612400031X/pdfft?md5=c09976a177a807ea7c2d8cb942485491&pid=1-s2.0-S277297612400031X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142149210","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":"Sex differences in cardiac mitochondrial respiration and reactive oxygen species production may predispose Scn1a−/+ mice to cardiac arrhythmias and Sudden Unexpected Death in Epilepsy","authors":"Jessa L. Aldridge,&nbsp;Emily Davis Alexander,&nbsp;Allison A. Franklin,&nbsp;Elizabeth Harrington,&nbsp;Farah Al-Ghzawi,&nbsp;Chad R. Frasier","doi":"10.1016/j.jmccpl.2024.100090","DOIUrl":"10.1016/j.jmccpl.2024.100090","url":null,"abstract":"<div><p>Dravet Syndrome (DS) is a pediatric-onset epilepsy with an elevated risk of Sudden Unexpected Death in Epilepsy (SUDEP). Most individuals with DS possess mutations in the voltage-gated sodium channel gene <em>Scn1a</em>, expressed in both the brain and heart. Previously, mutations in <em>Scn1a</em> have been linked to arrhythmia. We used a <em>Scn1a</em>^{<em>−/+</em>} DS mouse model to investigate changes to cardiac mitochondrial function that may underlie arrhythmias and SUDEP. We detected significant alterations in mitochondrial bioenergetics that were sex-specific. Mitochondria from male <em>Scn1a</em>^−/+ hearts had deficits in maximal (<em>p</em> = 0.02) and Complex II-linked respiration (<em>p</em> = 0.03). Male <em>Scn1a</em>^{<em>−/+</em>} mice were also more susceptible to cardiac arrhythmias under increased workload. When isolated cardiomyocytes were subjected to diamide, cardiomyocytes from male <em>Scn1a</em>^{<em>−/+</em>} hearts were less resistant to thiol oxidation. They had decreased survivability compared to <em>Scn1a</em>^<em>+/+</em> (<em>p</em> = 0.02) despite no whole-heart differences. Lastly, there were no changes in mitochondrial ROS production between DS and wild-type mitochondria at basal conditions, but <em>Scn1a</em>^{<em>−/+</em>} mitochondria accumulated more ROS during hypoxia/reperfusion. This study determines novel sex-linked differences in mitochondrial and antioxidant function in <em>Scn1a</em>-linked DS. Importantly, we found that male <em>Scn1a</em>^{<em>−/+</em>} mice are more susceptible to cardiac arrhythmias than female <em>Scn1a</em>^{<em>−/+</em>} mice. When developing new therapeutics to address SUDEP risk in DS, sex should be considered.</p></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"9 ","pages":"Article 100090"},"PeriodicalIF":0.0,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772976124000308/pdfft?md5=2da615d16145cdfd13dc6d32f23a5506&pid=1-s2.0-S2772976124000308-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142041131","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}