Anna Wolska, Yeganeh Mansourian, Rafael Zubirán, Maureen Sampson, Alan T Remaley
{"title":"New Methods for Calculating LDL-Cholesterol and Related Biomarkers of Atherosclerotic Cardiovascular Disease Risk.","authors":"Anna Wolska, Yeganeh Mansourian, Rafael Zubirán, Maureen Sampson, Alan T Remaley","doi":"10.1007/s11883-026-01398-z","DOIUrl":"10.1007/s11883-026-01398-z","url":null,"abstract":"","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"28 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12935843/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147282832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Farshad Heydari, Michael R Hamblin, Jalal Naghinezhad
{"title":"From Inflammation to Targeted Therapy: Leveraging Neutrophil, Platelet, RBC, and Macrophage Biology for Nanocarrier in Atherosclerosis.","authors":"Farshad Heydari, Michael R Hamblin, Jalal Naghinezhad","doi":"10.1007/s11883-026-01394-3","DOIUrl":"https://doi.org/10.1007/s11883-026-01394-3","url":null,"abstract":"","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"28 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147282822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Seungyeon Yeon, Sai-Wang Seto, Jyoti Deep Bhuyan, Dennis Chang, Chun Guang Li, Mitchell Low
{"title":"Sclerostin in Vascular Calcification: Hypoxia-Driven Regulation and Therapeutic Modulation by Natural Products.","authors":"Seungyeon Yeon, Sai-Wang Seto, Jyoti Deep Bhuyan, Dennis Chang, Chun Guang Li, Mitchell Low","doi":"10.1007/s11883-025-01377-w","DOIUrl":"10.1007/s11883-025-01377-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>Vascular calcification (VC) is increasingly recognized as an actively regulated pathological process rather than passive mineral deposition, strongly associated with aging, atherosclerosis, and chronic kidney disease. Sclerostin, a Wnt signalling antagonist primarily expressed in osteocytes, has recently been implicated in VC, although its precise vascular role remains debated. This review aims to integrate mechanistic and translational evidence on how hypoxia and hypoxia-inducible factor-1α (HIF-1α) regulate sclerostin and contribute to vascular mineralisation.</p><p><strong>Recent findings: </strong>Experimental studies demonstrate that HIF-1α activation links hypoxia to key osteogenic pathways, including BMP2, RUNX2, and Wnt/β-catenin signalling, thereby influencing phenotypic switching of vascular smooth muscle cells (VSMCs). Hypoxia exerts both stimulatory and suppressive effects on sclerostin depending on local tissue conditions, reflecting a context-dependent regulatory network. Preclinical and clinical data show that sclerostin can act as either a compensatory inhibitor or a pro-calcific mediator, depending on disease stage and metabolic environment. Emerging evidence further highlights natural products such as polyphenols, flavonoids, and marine-derived compounds that modulate sclerostin expression through oxidative, inflammatory, and Wnt-related pathways. Sclerostin sits at a critical intersection between bone and vascular systems, where hypoxia-driven HIF signalling orchestrates its dual effects on mineral metabolism. Understanding the HIF-sclerostin axis provides new insight into the bone-vascular continuum and identifies potential therapeutic targets. Natural bioactive compounds capable of restoring sclerostin-Wnt balance may represent safe, multi-targeted strategies to mitigate VC progression, warranting further mechanistic and translational evaluation.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"28 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12929286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147269970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Surfactant Protein B and the Lung-HDL-Vascular Axis: Linking Pulmonary Injury to Cardiovascular Risk.","authors":"Baohai Shao","doi":"10.1007/s11883-026-01391-6","DOIUrl":"https://doi.org/10.1007/s11883-026-01391-6","url":null,"abstract":"","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"28 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146257448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tanesh Ayyalu, Tia Bimal, Maya S Safarova, Zohaib M Bagha, Allen J Taylor, Peter P Toth
{"title":"Correction: Beyond LDL Cholesterol Reduction: Pleiotropic Profiling of Statins.","authors":"Tanesh Ayyalu, Tia Bimal, Maya S Safarova, Zohaib M Bagha, Allen J Taylor, Peter P Toth","doi":"10.1007/s11883-026-01397-0","DOIUrl":"https://doi.org/10.1007/s11883-026-01397-0","url":null,"abstract":"","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"28 1","pages":"23"},"PeriodicalIF":5.2,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Elias Björnson, Martin Adiels, Marja-Riitta Taskinen, Chris J Packard, Jan Borén
{"title":"Apolipoprotein C-III: Risk-factor, Regulator of Triglyceride-rich Lipoprotein Metabolism and Therapeutic Target.","authors":"Elias Björnson, Martin Adiels, Marja-Riitta Taskinen, Chris J Packard, Jan Borén","doi":"10.1007/s11883-026-01399-y","DOIUrl":"10.1007/s11883-026-01399-y","url":null,"abstract":"","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"28 1","pages":"22"},"PeriodicalIF":5.2,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12909363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146200417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Diana De Oliveira-Gomes, Alfonso Martinez de Majo, Angie Ardila-Delgado, Sara S Inglis, Stacy A Mandras, Juan F Loro-Ferrer, Adrian daSilva-deAbreu
{"title":"Cardio-Obesity and Therapeutic Advances: Intersections Between Excess Adiposity, Cardiovascular Risk, and Pharmacologic Interventions.","authors":"Diana De Oliveira-Gomes, Alfonso Martinez de Majo, Angie Ardila-Delgado, Sara S Inglis, Stacy A Mandras, Juan F Loro-Ferrer, Adrian daSilva-deAbreu","doi":"10.1007/s11883-026-01395-2","DOIUrl":"https://doi.org/10.1007/s11883-026-01395-2","url":null,"abstract":"<p><strong>Purpose of review: </strong>This review examines the mechanistic pathways linking obesity and cardiovascular disease, with particular emphasis on recent advancements in pharmacologic therapies. It evaluates the cardiovascular effects of novel anti-obesity medications and their integration into current treatment paradigms. Additionally, these pharmacologic strategies are contextualized alongside lifestyle interventions and metabolic bariatric surgery.</p><p><strong>Recent findings: </strong>Incretin agonist therapies, including both glucagon-like peptide-1 (GLP-1) receptor agonists and dual GLP-1/glucose-dependent insulinotropic polypeptide (GIP) receptor agonists have shown substantial efficacy in weight reduction and cardiometabolic improvement. Clinical trials have demonstrated that these agents not only reduce body weight by 10-20% but also significantly lower the risk of major adverse cardiovascular events, including cardiovascular death, nonfatal myocardial infarction, and stroke. These benefits have been observed in both patients with and without diabetes mellitus, and the cardiovascular protection extends beyond glycemic control. Tirzepatide, in particular, has shown superior efficacy compared to GLP-1 monotherapy in weight loss. Pharmacologic therapy has become a central pillar in the management of obesity-related cardiovascular risk. The emergence of agents with proven efficacy in both weight reduction and cardiovascular outcome improvement marks a paradigm shift in treatment. These findings support early and sustained use of pharmacotherapy in high-risk individuals, highlighting a need for integrated, personalized care strategies in obesity management.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"28 1","pages":"21"},"PeriodicalIF":5.2,"publicationDate":"2026-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146178251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mirela Hendel, Martyna Gut-Misiaga, Aleksandra Gil, Hanna Kwiendacz, Benjamin Y Q Tan, Joanne L Fothergill, Janusz Gumprecht, Gregory Y H Lip, Katarzyna Nabrdalik
{"title":"Gut Microbiota and Stroke: New Insights into the Gut-Brain-Vascular Axis.","authors":"Mirela Hendel, Martyna Gut-Misiaga, Aleksandra Gil, Hanna Kwiendacz, Benjamin Y Q Tan, Joanne L Fothergill, Janusz Gumprecht, Gregory Y H Lip, Katarzyna Nabrdalik","doi":"10.1007/s11883-025-01381-0","DOIUrl":"https://doi.org/10.1007/s11883-025-01381-0","url":null,"abstract":"<p><strong>Purpose of review: </strong>Recent advances have underscored the importance of interactions between the gut microbiota, vascular system and brain in stroke pathogenesis. This review introduces the conceptual framework of the gut-brain-vascular axis and summarizes evidence on how microbiota affects neurovascular integrity and stroke outcomes via intricate immunological, metabolic and endothelial mechanisms.</p><p><strong>Recent findings: </strong>Recent clinical and epidemiological studies have demonstrated that specific profiles of gut microbiota are associated with stroke severity and clinical outcomes. Dysfunction of the gut barrier integrity and the translocation of endotoxins can induce low-grade systemic inflammation, which is a common mechanism underlying both cerebrovascular events and atherogenesis. Furthermore, microbial metabolites such as trimethylamine-N-oxide (TMAO), short-chain fatty acids (SCFAs) and bile acids (BAs) have been shown to modulate endothelial function, platelet hyperactivation and blood-brain barrier (BBB) permeability. Advances in BBB modelling reveal how microbial signals contribute to neurovascular dysfunction. Glycocalyx disruption, marked by elevated syndecan-1 (SDC1), reflects endothelial injury and could be used as a stroke biomarker. Furthermore, altered tryptophan metabolism via the kynurenine pathway is a contributing factor to neuroinflammation, thereby establishing a link between gut dysbiosis and cerebrovascular pathology. Emerging evidence on the gut-brain-vascular axis indicates that preventing dysbiosis may reduce stroke risk, while post-stroke modulation of the microbiota could enhance recovery. The gut-brain-vascular axis provides a novel and integrative model linking gut microbiota disfunction to neurovascular and atherosclerotic disease. Understanding these interconnected pathways may inform future approaches to risk stratification and cerebrovascular disease prevention and treatment.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"28 1","pages":"18"},"PeriodicalIF":5.2,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146092435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ting Sun, Zhihua Wang, Chuankai Zhang, Xu Xu, Yixin Zhang, Yutao Li, Changjun Yin, Sarajo K Mohanta, Andreas J R Habenicht
{"title":"Artery Tertiary Lymphoid Organs Establish Biological Platforms to Connect Atherosclerotic Plaques to the Brain.","authors":"Ting Sun, Zhihua Wang, Chuankai Zhang, Xu Xu, Yixin Zhang, Yutao Li, Changjun Yin, Sarajo K Mohanta, Andreas J R Habenicht","doi":"10.1007/s11883-025-01384-x","DOIUrl":"https://doi.org/10.1007/s11883-025-01384-x","url":null,"abstract":"<p><strong>Purpose of review: </strong>The ability of the nervous system to sense cues from medium and large arteries is critical for maintaining vascular integrity and function. However, there is currently no evidence that atherosclerotic plaques of arteries other than arterioles are directly hard-wired by axons to transmit signals to the brain or that efferent axons from the brain gain access to plaques. Yet, studies in experimental mice have shown that the outer connective tissue coat of arteries, i.e. the adventitia, adopts sentinel functions to indirectly and faithfully connect plaques to the brain forming artery brain circuits (ABCs). This review focuses on the adventitia as a site that establishes powerful biological platforms in the form of highly innervated neuroimmune cardiovascular interfaces (NICIs) and shows that these interfaces impact atherosclerosis progression.</p><p><strong>Recent findings: </strong>The discovery of several cardiovascular brain circuits over the last several years considerably expanded our understanding how neural circuits regulate artery and heart homeostasis and disease. These circuits release neurotransmitters to modify leukocyte trafficking, affect endothelial cells, control vascular smooth muscle cells (VSMCs) behavior, and regulate local inflammation. Moreover, vascular inflammation in turn reorganizes neural innervation in the adventitia suggesting that tripartite communication networks between the cardiovascular, the nervous and the immune systems impact disease progression. In atherosclerosis, the formation of artery tertiary lymphoid organs (ATLOs) represents a specific form of NICIs adjacent to atherosclerotic plaques. The ATLO-associated NICIs act as hubs to connect plaques to the brain via multisynaptic projections and receive signals from the brain to convey to the arteries. These insights reveal a previously underappreciated level of integration between neural, immune and vascular networks in the pathogenesis of cardiovascular diseases. In this review, we consider recent advances in neuroimmune and neurovascular interactions in atherosclerosis, with a particular focus on the mechanisms by which these pathways contribute to disease progression.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"28 1","pages":"19"},"PeriodicalIF":5.2,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146092358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}