{"title":"Incidence of Infective Endocarditis Post-TPVR with MELODY Valve in Pediatric Patients: A Systematic Review and Meta-Analysis.","authors":"Sruthi Veldurthy, Deepali Shrivastava, Farhat Majeed, Tooba Ayaz, Aqssa Munir, Ali Haider, Maneeth Mylavarapu","doi":"10.2174/011573403X324878240903045701","DOIUrl":"10.2174/011573403X324878240903045701","url":null,"abstract":"<p><strong>Introduction: </strong>Infective Endocarditis (IE) has emerged to be one of the most impactful adverse complications post-transcatheter procedures, especially Transcatheter Pulmonary Valve Replacement (TPVR). We conducted a systematic review and meta-analysis with the aim of identifying the incidence of IE post-TPVR with the MELODY valve in the pediatric population.</p><p><strong>Methods: </strong>A comprehensive literature search was performed across several prominent databases, including PubMed/MEDLINE, SCOPUS, and Science Direct. Studies compared the clinical outcomes of pediatric patients who received TPVR using the MELODY valve. Data extraction was done for variables like the total pediatric patient population that underwent TPVR with MELODY valve, mean age, the sex of the patients, the incidence rate of IE following the procedure, and the duration between the procedure and the occurrence of IE. Inverse Variance was used to estimate the incidence of IE in patients who underwent TPVR with respective 95% confidence interval (CI).</p><p><strong>Results: </strong>In total, 4 studies with 414 pediatric patients who underwent TPVR using the MELODY valve were included in the study. The mean age of the study population was 12.7 ± 3.11 years. The pooled incidence of IE following TPVR with MELODY valve in the pediatric population was 17.70% (95% Cl 3.84-31.55; p<0.00001). Additionally, the mean length of duration to develop IE following TPVR with MELODY valve in the pediatric population was 2.18 years (95% Cl 0.35-4.01; p<0.00001).</p><p><strong>Conclusion: </strong>Our meta-analysis reveals that IE post-TPVR with MELODY valve in pediatric patients is a significant complication, clinically and statistically. Further research needs to be done to understand the risk factors and develop better management strategies.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":"e1573403X324878"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12060908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281688","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}
Amie Marie Kolimas, Gargya Malla, Abhimanyu Chadha, Enkhtsogt Sainbayar, Joshua Sethi, Ziad Hindosh, Priyanka Hadvani, Hoang Nhat Pham, Juan Sordia
{"title":"Slowing Thoracic Aortic Aneurysm Growth with Statins: A Meta-Analysis.","authors":"Amie Marie Kolimas, Gargya Malla, Abhimanyu Chadha, Enkhtsogt Sainbayar, Joshua Sethi, Ziad Hindosh, Priyanka Hadvani, Hoang Nhat Pham, Juan Sordia","doi":"10.2174/011573403X343512250127075044","DOIUrl":"10.2174/011573403X343512250127075044","url":null,"abstract":"<p><strong>Introduction: </strong>Thoracic aortic aneurysms (TAAs) are worrisome for their propensity to dissect. Previous studies have demonstrated the potential benefits of statin use, particularly with slowing aortic aneurysm growth. The aim of this meta-analysis was to consolidate existing research to ascertain if statins effectively reduce TAA growth.</p><p><strong>Methods: </strong>Multiple databases were searched to identify studies assessing TAA growth in patients on statins (cases) and those not on statins (controls). The primary outcome was TAA (ascending/ aortic arch) growth rate per year. Standard mean difference (SMD) and 95% confidence intervals (95% CI) were estimated with a random-effects model using the inverse-variance technique. We assigned I2>50% as an indicator of statistical heterogeneity. P-value <0.05 was considered significant. Data analysis was performed using SPSS v.25.0.</p><p><strong>Results: </strong>Four studies comprising 757 cases (male 64%, mean age 65±14 years) and 1,696 controls (male 62%, mean age 61±18 years) were included. The baseline diameters of TAA for cases and controls were 40.35±8.75 mm and 42.39±12.60 mm, respectively. Pooled results suggested statins to be associated with slower growth of TAAs with pooled SMD -0.70 mm/year [95% CI (-1.23 - -0.16); p=0.01]. Heterogeneity statistics among 4 studies was 95%.</p><p><strong>Conclusion: </strong>This pooled meta-analysis showed statins as associated with slower growth of TAAs. However, given the heterogeneity of the included studies in this meta-analysis, results should be interpreted with caution.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":"112-116"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308008/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412954","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":"Diabetic Cardiomyopathy: An Update on Emerging Pathological Mechanisms.","authors":"Chirag Kakkar, Veerta Sharma, Ashi Mannan, Gaurav Gupta, Sachin Singh, Puneet Kumar, Kamal Dua, Amarjot Kaur, Shareen Singh, Sonia Dhiman, Thakur Gurjeet Singh","doi":"10.2174/011573403X331870241025094307","DOIUrl":"10.2174/011573403X331870241025094307","url":null,"abstract":"<p><p>Diabetic Cardiomyopathy (DCM) is a notable consequence of diabetes mellitus, distinguished by cardiac dysfunction that occurs separately from coronary artery disease or hypertension. A recent study has revealed an intricate interaction of pathogenic processes that contribute to DCM. Important aspects involve the dysregulation of glucose metabolism, resulting in heightened oxidative stress and impaired mitochondrial function. In addition, persistent high blood sugar levels stimulate inflammatory pathways, which contribute to the development of heart fibrosis and remodelling. Additionally, changes in the way calcium is managed and the presence of insulin resistance are crucial factors in the formation and advancement of DCM. This may be due to the involvement of many molecular mechanistic pathways such as NLRP3, NF-κB, PKC, and MAPK with their downstream associated signaling pathways. Gaining a comprehensive understanding of these newly identified pathogenic pathways is crucial in order to design precise therapy approaches that can enhance the results for individuals suffering from diabetes. In addition, this review offers an in-depth review of not just pathogenic pathways and molecular mechanistic pathways but also diagnostic methods, treatment options, and clinical trials.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":"e1573403X331870"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12060924/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582221","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}
April Olson, Hoang Nhat Pham, Ramzi Ibrahim, Mohammed Salih, Amitoj Singh, Mamas A Mamas
{"title":"Disparities in Peripheral Artery Disease-related Mortality in Chronic Inflammatory Disease in the United States from 1999 to 2020.","authors":"April Olson, Hoang Nhat Pham, Ramzi Ibrahim, Mohammed Salih, Amitoj Singh, Mamas A Mamas","doi":"10.2174/011573403X353038241125050631","DOIUrl":"10.2174/011573403X353038241125050631","url":null,"abstract":"<p><strong>Introduction: </strong>Peripheral arterial disease (PAD) is a marker of significant atherosclerotic cardiovascular disease and is associated with greater healthcare burden and worse prognosis in individuals with chronic inflammatory disease (CID). We aimed to investigate temporal trends and disparities of PAD-related mortality in populations with CID from 1999-2020 across six common CIDs (i.e., chronic viral hepatitis, human immunodeficiency virus, inflammatory bowel disease, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus).</p><p><strong>Methods: </strong>United States (US) PAD and CID-related mortality and demographic data from 1999- 2020 were extracted from the CDC database through the multiple-cause-of-death files. Ageadjusted mortality rates (AAMR) per 1,000,000 and 95% confidence intervals were standardized to the 2000 US population. The mortality trends were analyzed using Joinpoint Regression.</p><p><strong>Results: </strong>A total of 22,175 PAD-related deaths were recorded in the population with CID between 1999 and 2020. Mortality remained stable during the 22-year period (AAPC -0.04%, p=0.95) with a cumulative AAMR of 4.64. Mortality was highest in rural counties (AAMR 5.27), and among non-Hispanic Black populations (AAMR 7.06). Among the CID subtypes, PAD mortality was highest in populations with RA (AAMR 2.48) and lowest in populations with psoriasis (AAMR 0.11).</p><p><strong>Conclusion: </strong>Our findings highlight the disparities of PAD mortality in patients with CID, with the Black population and rural communities disproportionately affected. Further investigation with individual- level data is warranted to identify the contributing factors for the observed disparities.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":"e1573403X353038"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12172234/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806328","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":"Hot Water Immersion as a Means to Prevent Cardiovascular Disease and Associated Mortality.","authors":"Metodija Kjertakov, Aaron Petersen","doi":"10.2174/011573403X319557240822094347","DOIUrl":"10.2174/011573403X319557240822094347","url":null,"abstract":"<p><p>Physical activity is widely promoted as a preventive strategy against cardiovascular disease and death from this disease. However, the fact that some individuals are unable or unwilling to engage in physical activity highlights the need for alternative strategies. Passive heat exposure using hot water immersion could serve as an alternative to physical exercise, as it provides similar, if not greater, cardioprotection than physical activity. This perspective article presents evidence supporting our concept and provides recommendations for hot water immersion sessions.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":"e1573403X319557"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12060910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055166","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":"Identifying Biomarkers for Atherosclerosis via Gene Expression and Biological Networking.","authors":"Sangeeta Chhotaray, Soumya Jal","doi":"10.2174/011573403X340118241113025519","DOIUrl":"10.2174/011573403X340118241113025519","url":null,"abstract":"<p><strong>Introduction: </strong>Atherosclerosis is a chronic disease caused by the accumulation of lipids, inflammatory cells, and fibrous elements in arterial walls, leading to plaque formation and cardiovascular conditions like coronary artery disease, stroke, and peripheral arterial disease. Factors like hyperlipidemia, hypertension, smoking, and diabetes contribute to its development. Diagnosis relies on imaging and biomarkers, while management includes lifestyle modifications, pharmacotherapy, and surgical interventions. Computational biology is transforming biological knowledge into clinical practice by identifying biomarkers that can predict clinical outcomes. This involves omics data, predictive modeling, and data integration. Statistical analysis-based methods are also being developed to develop and integrate methods for screening, diagnosing, and prognosing atherosclerosis.</p><p><strong>Methodology: </strong>The present work aimed to uncover critical genes and pathways to enhance the understanding of the mechanism of atherosclerosis. GSE23746 was analyzed to find differentially expressed genes (DEGs) using 19 control samples and 76 atherosclerotic samples.</p><p><strong>Results: </strong>A total of 76 DEGs were identified. Analysed DEGs using Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) to generate enrichment datasets. A Protein- protein Interaction (PPI) network of DEGs was created utilizing the Search Tool for the Retrieval of Interacting Genes (STRING).</p><p><strong>Conclusion: </strong>Ten hub genes, namely EGR1, PTGS2, TNF, NFKBIA, CXCL8, TNFAIP3, CCL3, IL1B, PTPRC, and CD83, were found to be significantly linked to atherosclerosis. Furthermore, the metabolic pathway analysis through KEGG and STRING provides potential targets for therapeutic interventions through HUB genes to diagnose the illness at an early stage, which aids in the reduction of cardiovascular risk. From risk factor profiling to the discovery of novel biomarkers, several components such as phospholipids, ANGPTL3, LCAT, and the proteinencoded OCT-1 gene, play a vital role in crucial processes. These compounds are potential therapeutic targets for early diagnosis of atherosclerotic lesions and future novel biomarkers.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":"e1573403X340118"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12172219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142946061","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":"Importance of Zinc Homeostasis for Normal Cardiac Rhythm.","authors":"Pejman Kokhabi, Reza Mollazadeh, Seyedeh Fatemeh Hejazi, Aida Hossein Nezhad, Hamidreza Pazoki-Toroudi","doi":"10.2174/011573403X299868240904120621","DOIUrl":"10.2174/011573403X299868240904120621","url":null,"abstract":"<p><p>Current arrhythmia therapies such as ion channel blockers, catheter ablation, or implantable cardioverter defibrillators have limitations and side effects, and given the proarrhythmic risk associated with conventional, ion channel-targeted anti-arrhythmic drug therapies, a new approach to arrhythmias may be warranted. Measuring and adjusting the level of specific ions that impact heart rhythm can be a simple and low-complication strategy for preventing or treating specific arrhythmias. In addition, new medicines targeting these ions may effectively treat arrhythmias. Numerous studies have shown that intracellular and extracellular zinc concentrations impact the heart's electrical activity. Zinc has been observed to affect cardiac rhythm through a range of mechanisms. These mechanisms encompass the modulation of sodium, calcium, and potassium ion channels, as well as the influence on beta-adrenergic receptors and the enzyme adenylate cyclase. Moreover, zinc can either counteract or induce oxidative stress, hinder calmodulin or the enzyme Ca (<sup>2+</sup>)/calmodulin-dependent protein kinase II (CaMKII), regulate cellular ATP levels, affect the processes of aging and autophagy, influence calcium ryanodine receptors, and control cellular inflammation. Additionally, zinc has been implicated in the modulation of circadian rhythm. In all the aforementioned cases, the effect of zinc on heart rhythm is largely influenced by its intracellular and extracellular concentrations. Optimal zinc levels are essential for maintaining a normal heart rhythm, while imbalances-whether deficiencies or excesses-can disrupt electrical activity and contribute to arrhythmias.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":"e1573403X299868"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12060914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281687","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}
Luiz Fernando Leite da Silva Neto, Adriano Leitao de Almeida, Leticia Fonseca Macedo, Caua Leal do Espírito Santo, Caio Vinicius Botelho Brito, Renato Garcia Lisboa Borges
{"title":"The Impact of Beta-Blocker Maintenance on Decompensated Heart Failure: A Systematic Review and Meta-Analysis.","authors":"Luiz Fernando Leite da Silva Neto, Adriano Leitao de Almeida, Leticia Fonseca Macedo, Caua Leal do Espírito Santo, Caio Vinicius Botelho Brito, Renato Garcia Lisboa Borges","doi":"10.2174/011573403X291307240902071924","DOIUrl":"10.2174/011573403X291307240902071924","url":null,"abstract":"<p><strong>Background: </strong>Acute Heart Failure (HF) is related to a significant hospital mortality rate and functional impairment in many patients. However, there is still a lack of studies that support the use of Beta-blockers (BB) in the management of decompensated HF.</p><p><strong>Objective: </strong>This study aimed to evaluate the impact on mortality of maintaining BB in patients with decompensated HF.</p><p><strong>Methods: </strong>A systematic review and meta-analysis was performed, using the databases PubMed, Cochrane Library, SCIELO and BVS, selecting only cohort studies and Randomized Clinical Trials (RCTs) from the last 10 years, which have been selected based on inclusion and exclusion criteria.</p><p><strong>Results: </strong>An 86% reduction in the risk of in-hospital death was found (RR=0.14, 95% CI: 0.10- 0.18) in patients with HF who maintained the use of BB during hospitalization. A second analysis found a 44% (RR=0.56, 95% CI: 0.47-0.66) lower chance of in-hospital death in the group that previously used BB. Regarding the analysis of mortality after hospital discharge, only studies that have evaluated the use of BB in HF with reduced ejection fraction pointed to a reduction in mortality. Furthermore, some articles have found a relationship between the reduction in readmissions and the use of post-discharge BB.</p><p><strong>Conclusion: </strong>There is still no consensus regarding the use of BB in patients hospitalized with decompensated HF. In view of the limitations of the data found in the present study, the need for more RCTs that address this topic is emphasized in order to resolve this uncertainty in the management of cardiovascular patients.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":"e1573403X291307"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12060926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142281689","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":"Leptin Resistance and Cardiometabolic Disorders: Bridging Molecular Pathways, Genetic Variants, and Therapeutic Innovation.","authors":"Prashanjit Roy, Rishi Kant, Amandeep Kaur, Hardik Kumar, Ranjeet Kumar","doi":"10.2174/011573403X356019250118170444","DOIUrl":"10.2174/011573403X356019250118170444","url":null,"abstract":"<p><p>Leptin, a hormone produced by fat cells, is crucial for regulating energy equilibrium, managing body mass, and influencing metabolic and cardiovascular well-being. Leptin decreases appetite, boosts energy usage, and has a significant impact on glucose metabolism by primarily activating the JAK2/STAT3 signaling pathway in the hypothalamus. Obesity leads to the development of leptin resistance, which is marked by high levels of leptin in the bloodstream and a decreased responsiveness to its signals. This leads to increased food consumption, weight gain, and metabolic issues, such as type 2 diabetes (T2DM) and cardiovascular disease (CVD). This study explores the many roles of leptin in metabolic regulation, with a specific emphasis on its interaction with insulin and its impact on peripheral organs like the pancreas, liver, and muscles. Leptin resistance worsens chronic inflammation, oxidative stress, endothelial dysfunction, and insulin resistance, all of which are strongly linked to the development of cardiovascular disease (CVD). Moreover, there is a correlation between genetic variations in the leptin receptor (LEPR) gene and a higher susceptibility to stroke and other cardiovascular issues. Therapeutic interventions, such as leptin replacement therapy, have demonstrated potential in the treatment of congenital leptin insufficiency and lipodystrophy while also enhancing glycaemic control, lipid profiles, and neuroendocrine function. Recent studies have indicated that manipulating leptin levels or enhancing its responsiveness by specific treatments, such as chemical chaperones and inhibitors of negative regulators like SOCS3 and PTP1B, might potentially restore the efficacy of leptin.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":"52-67"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12307987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390356","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}
Seyed Mehdi Mousavi, Fatemeh Jalali-Zefrei, Mohammad Shourmij, Shiva Tabaghi, Amirhesam Davari, Saeed Bahador Khalili, Soghra Farzipour, Arsalan Salari
{"title":"Targeting Wnt Pathways with Small Molecules as New Approach in Cardiovascular Disease.","authors":"Seyed Mehdi Mousavi, Fatemeh Jalali-Zefrei, Mohammad Shourmij, Shiva Tabaghi, Amirhesam Davari, Saeed Bahador Khalili, Soghra Farzipour, Arsalan Salari","doi":"10.2174/011573403X333038241023153349","DOIUrl":"10.2174/011573403X333038241023153349","url":null,"abstract":"<p><p>The increasing incidences of morbidity and mortality associated with cardiovascular diseases represent significant difficulties for clinical treatment and have a major impact on patient health. Wnt signaling pathways are highly conserved and are well known for their regulatory roles in embryonic development, tissue regeneration, and adult tissue homeostasis. Wnt signaling is classified into two distinct pathways: canonical Wnt/β-catenin signaling and noncanonical pathways, including planar cell polarity and Wnt/Ca<sup>2+</sup> pathways. A growing body of experimental evidence suggests the involvement of both canonical and non-canonical Wnt signaling pathways in the development of cardiovascular diseases, including myocardial hypertrophy, arrhythmias, diabetic cardiomyopathy, arrhythmogenic cardiomyopathy, and myocardial infarction. Thus, to enhance patient quality of life, diagnosing and treating cardiac illnesses may require a thorough understanding of the molecular functions played by the Wnt pathway in these disorders. Many small-molecule inhibitors specifically target various components within the Wnt signaling pathways, such as Frizzled, Disheveled, Porcupine, and Tankyrase. This study aims to present an overview of the latest findings regarding the functions of Wnt signaling in human cardiac disorders and possible inhibitors of Wnt, which could lead to novel approaches for treating cardiac ailments.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":"e1573403X333038"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12060913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557353","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}