Basic Research in Cardiology最新文献

Assessing customized multivalent chemokine-binding peptide treatment in a murine model of coxsackievirus B3 myocarditis

IF 9.5 1区医学

Basic Research in Cardiology Pub Date : 2025-02-26 DOI: 10.1007/s00395-025-01098-w

Nicolas Kelm, Meike Kespohl, Gintare Smagurauskaite, Serena Vales, Kalimuthu Karuppanan, Philomena Mburu, Arne Thiele, Sandra Pinkert, Thomas Bukur, Michael Mülleder, Nikolaus Berndt, Karin Klingel, Matthias M. Gaida, Shoumo Bhattacharya, Antje Beling

{"title":"Assessing customized multivalent chemokine-binding peptide treatment in a murine model of coxsackievirus B3 myocarditis","authors":"Nicolas Kelm, Meike Kespohl, Gintare Smagurauskaite, Serena Vales, Kalimuthu Karuppanan, Philomena Mburu, Arne Thiele, Sandra Pinkert, Thomas Bukur, Michael Mülleder, Nikolaus Berndt, Karin Klingel, Matthias M. Gaida, Shoumo Bhattacharya, Antje Beling","doi":"10.1007/s00395-025-01098-w","DOIUrl":"https://doi.org/10.1007/s00395-025-01098-w","url":null,"abstract":"Myocarditis, an inflammatory disease of the heart muscle, is often triggered by viral infections. This inflammation, which can lead to severe cardiac dysfunction and adverse outcomes, is mediated by various CC and CXC chemokines that interact with receptors in a “one-to-many” fashion. Ticks have evolved chemokine-binding salivary proteins known as Evasins, which efficiently suppress inflammation. This study explores a tailored Evasin-derived CC chemokine-targeting strategy using a 17-mer synthetic dimeric peptide, BK1.3. This peptide inhibits the inflammatory chemokines CCL2, CCL3, CCL7, and CCL8 in murine Coxsackievirus B3 (CVB3) infection, a viral trigger of myocarditis. Administered at a dose of 5 mg/kg twice daily, BK1.3 effectively maintains virus control without exacerbating CVB3-induced morbidity markers, such as hemodynamic compromise, multiorgan failure with hepatitis and pancreatitis, hypothermia, hypoglycemia, and weight loss. Metabolic profiling combined with proteomics reveals preserved reprogramming of lipid storage and gluconeogenesis capacity in the liver, alongside sustained energy production in the injured heart muscle. In survivors of acute CVB3 infection exhibiting manifestations of the subacute phase, BK1.3 enhances virus control, reduces myeloid cell infiltration in the heart and liver, improves markers of liver injury, and alleviates cardiac dysfunction, as evidenced by echocardiographic global longitudinal strain analysis. These findings affirm the safety profile of BK1.3 peptide therapeutics in a preclinical mouse model of acute CVB3 infection and emphasize its potential for therapeutic advancement in addressing virus-induced inflammation in the heart.","PeriodicalId":8723,"journal":{"name":"Basic Research in Cardiology","volume":"27 1","pages":""},"PeriodicalIF":9.5,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143495156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Associations between female sex hormones, estrous cycle, ischemic preconditioning and myocardial infarct size after ischemia–reperfusion injury

IF 9.5 1区医学

Basic Research in Cardiology Pub Date : 2025-02-13 DOI: 10.1007/s00395-025-01099-9

Tetiana Pylova, Ahmed Elmahdy, Maryna Krasnikova, Abhishek Jha, Erik Axel Andersson, Yalda Kakaei, Aaron Shekka Espinosa, Amin Al-Awar, Ermir Zulfaj, Amirali Nejat, Valentyna Sevastianova, Mana Kalani, Henrik Ryberg, Åsa Tivesten, Elmir Omerovic, Björn Redfors

{"title":"Associations between female sex hormones, estrous cycle, ischemic preconditioning and myocardial infarct size after ischemia–reperfusion injury","authors":"Tetiana Pylova, Ahmed Elmahdy, Maryna Krasnikova, Abhishek Jha, Erik Axel Andersson, Yalda Kakaei, Aaron Shekka Espinosa, Amin Al-Awar, Ermir Zulfaj, Amirali Nejat, Valentyna Sevastianova, Mana Kalani, Henrik Ryberg, Åsa Tivesten, Elmir Omerovic, Björn Redfors","doi":"10.1007/s00395-025-01099-9","DOIUrl":"https://doi.org/10.1007/s00395-025-01099-9","url":null,"abstract":"Studies on sex differences in myocardial infarction (MI) typically focus on males versus females, the exploration of hormonal physiologic variations and their impact on the infarct size remains limited. The objective of this study was to examine whether infarct size after myocardial ischemia/reperfusion injury in female rats differs in different phases of the estrous cycle, and according to the levels of sex hormones; and to assess whether the effect of ischemic preconditioning on infarct size varies in different phases of the estrous cycle and between sexes. Female rats were divided into three groups based on the estrous cycle: proestrus, estrus, and diestrus. A fourth group consisted of ovariectomized female rats. Male rats were included as a fifth group, and orchiectomized males as a sixth group. Each group underwent ischemia/reperfusion injury, with or without prior ischemic preconditioning (IPC). Plasma sex hormone levels were measured with gas chromatography-tandem mass spectrometry. Females in the proestrus showed significantly smaller infarct size compared to all other groups. Multivariable analyses identified proestrus, IPC, and estradiol as independent predictors of smaller infarct size while male sex and gonadectomy as independent predictors of larger infarct size. There was a statistical interaction between IPC and both sex and hormonal status, with a greater protective effect of IPC on infarct size in males and gonadectomized rats. After ischemia–reperfusion, proestrus female rats developed the smallest while male and gonadectomized rats the largest infarct size. Conversely, IPC conferred greater cardioprotection in male and gonadectomized rats than females in proestrus.","PeriodicalId":8723,"journal":{"name":"Basic Research in Cardiology","volume":"7 1","pages":""},"PeriodicalIF":9.5,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143401933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Evolocumab attenuates myocardial ischemia/reperfusion injury by blocking PCSK9/LIAS-mediated cuproptosis of cardiomyocytes

IF 9.5 1区医学

Basic Research in Cardiology Pub Date : 2025-02-11 DOI: 10.1007/s00395-025-01100-5

Zi-Zhuo Li, Lei Guo, Yan-Liang An, Wei-Jia Yu, Ding-Yu Shi, Qiu-Yue Lin, Bo Zhang

{"title":"Evolocumab attenuates myocardial ischemia/reperfusion injury by blocking PCSK9/LIAS-mediated cuproptosis of cardiomyocytes","authors":"Zi-Zhuo Li, Lei Guo, Yan-Liang An, Wei-Jia Yu, Ding-Yu Shi, Qiu-Yue Lin, Bo Zhang","doi":"10.1007/s00395-025-01100-5","DOIUrl":"https://doi.org/10.1007/s00395-025-01100-5","url":null,"abstract":"Myocardial ischemia‒reperfusion (I/R) injury is the crucial cause of poor prognosis after revascularization in patients with myocardial infarction (MI) due to the lack of specific therapeutic drugs. Proprotein convertase subtilisin/Kexin type 9 (PCSK9) is related to the pathogenesis and progression of various cardiovascular diseases. However, the specific role of PCSK9 in I/R-induced cardiac injury remains to be further investigated. In this study, wild-type (WT) C57BL/6J mice were administered evolocumab (a monoclonal antibody of PCSK9) before I/R surgery. Cardiac damage and function were assessed by echocardiography and TTC/Evans Blue staining. Inflammation, oxidative stress, mitochondrial dysfunction, and cuproptosis were evaluated by histopathology and qPCR. The interaction between proteins was confirmed by protein docking and co-immunoprecipitation. Our data revealed that PCSK9 level was increased in I/R-induced mouse serum and hearts and in serum of MI patients. Furthermore, evolocumab significantly improved cardiac injury and dysfunction, inflammation, oxidative stress, and cuproptosis. Mechanistically, evolocumab obstructs the direct interaction of PCSK9 and LIAS, and subsequently inhibits cardiomyocyte cuproptosis. In conclusion, inhibition of PCSK9 alleviates I/R-induced cardiac remodeling and dysfunction by targeting LIAS-mediated cuproptosis, which may be a novel therapeutic strategy for patients with ischemic cardiomyopathy.","PeriodicalId":8723,"journal":{"name":"Basic Research in Cardiology","volume":"29 1","pages":""},"PeriodicalIF":9.5,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143385124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role and mechanism of epigenetics in anticancer drug-induced cardiotoxicity. 表观遗传学在抗癌药物诱导的心脏毒性中的作用和机制。

IF 7.5 1区医学

Basic Research in Cardiology Pub Date : 2025-02-01 Epub Date: 2024-05-09 DOI: 10.1007/s00395-024-01054-0

Xuening Liu, Zijian Li

引用次数: 0

Molecular fingerprints of cardiovascular toxicities of immune checkpoint inhibitors. 免疫检查点抑制剂心血管毒性的分子指纹。

IF 7.5 1区医学

Basic Research in Cardiology Pub Date : 2025-02-01 Epub Date: 2024-07-17 DOI: 10.1007/s00395-024-01068-8

Tamás G Gergely, Zsófia D Drobni, Nabil V Sayour, Péter Ferdinandy, Zoltán V Varga

{"title":"Molecular fingerprints of cardiovascular toxicities of immune checkpoint inhibitors.","authors":"Tamás G Gergely, Zsófia D Drobni, Nabil V Sayour, Péter Ferdinandy, Zoltán V Varga","doi":"10.1007/s00395-024-01068-8","DOIUrl":"10.1007/s00395-024-01068-8","url":null,"abstract":"Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy by unleashing the power of the immune system against malignant cells. However, their use is associated with a spectrum of adverse effects, including cardiovascular complications, which can pose significant clinical challenges. Several mechanisms contribute to cardiovascular toxicity associated with ICIs. First, the dysregulation of immune checkpoints, such as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein-1 (PD-1) and its ligand (PD-L1), and molecular mimicry with cardiac autoantigens, leads to immune-related adverse events, including myocarditis and vasculitis. These events result from the aberrant activation of T cells against self-antigens within the myocardium or vascular endothelium. Second, the disruption of immune homeostasis by ICIs can lead to autoimmune-mediated inflammation of cardiac tissues, manifesting as cardiac dysfunction and heart failure, arrhythmias, or pericarditis. Furthermore, the upregulation of inflammatory cytokines, particularly tumor necrosis factor-alpha, interferon-γ, interleukin-1β, interleukin-6, and interleukin-17 contributes to cardiac and endothelial dysfunction, plaque destabilization, and thrombosis, exacerbating cardiovascular risk on the long term. Understanding the intricate mechanisms of cardiovascular side effects induced by ICIs is crucial for optimizing patient care and to ensure the safe and effective integration of immunotherapy into a broader range of cancer treatment protocols. The clinical implications of these mechanisms underscore the importance of vigilant monitoring and early detection of cardiovascular toxicity in patients receiving ICIs. Future use of these key pathological mediators as biomarkers may aid in prompt diagnosis of cardiotoxicity and will allow timely interventions.","PeriodicalId":8723,"journal":{"name":"Basic Research in Cardiology","volume":" ","pages":"187-205"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141632513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exercise, cancer, and the cardiovascular system: clinical effects and mechanistic insights. 运动、癌症和心血管系统：临床效果和机理认识。

IF 7.5 1区医学

Basic Research in Cardiology Pub Date : 2025-02-01 Epub Date: 2024-02-14 DOI: 10.1007/s00395-024-01034-4

Simon Wernhart, Tienush Rassaf

{"title":"Exercise, cancer, and the cardiovascular system: clinical effects and mechanistic insights.","authors":"Simon Wernhart, Tienush Rassaf","doi":"10.1007/s00395-024-01034-4","DOIUrl":"10.1007/s00395-024-01034-4","url":null,"abstract":"Cardiovascular diseases and cancer are the leading causes of death in the Western world and share common risk factors. Reduced cardiorespiratory fitness (CRF) is a major determinant of cardiovascular morbidity and cancer survival. In this review we discuss cancer- induced disturbances of parenchymal, cellular, and mitochondrial function, which limit CRF and may be antagonized and attenuated through exercise training. We show the impact of CRF on cancer survival and its attenuating effects on cardiotoxicity of cancer-related treatment. Tailored exercise programs are not yet available for each tumor entity as several trials were performed in heterogeneous populations without adequate cardiopulmonary exercise testing (CPET) prior to exercise prescription and with a wide variation of exercise modalities. There is emerging evidence that exercise may be a crucial pillar in cancer treatment and a tool to mitigate cardiotoxic treatment effects. We discuss modalities of aerobic exercise and resistance training and their potential to improve CRF in cancer patients and provide an example of a periodization model for exercise training in cancer.","PeriodicalId":8723,"journal":{"name":"Basic Research in Cardiology","volume":" ","pages":"35-55"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139728833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cardioprotection of voluntary exercise against breast cancer-induced cardiac injury via STAT3. 自愿运动通过 STAT3 对乳腺癌诱发的心脏损伤起到保护作用

IF 7.5 1区医学

Basic Research in Cardiology Pub Date : 2025-02-01 Epub Date: 2024-08-19 DOI: 10.1007/s00395-024-01076-8

Lan Wu, Zhi-Zheng Li, Hao Yang, Li-Zhi Cao, Xiao-Ying Wang, Dong-Liang Wang, Emeli Chatterjee, Yan-Fei Li, Gang Huang

{"title":"Cardioprotection of voluntary exercise against breast cancer-induced cardiac injury via STAT3.","authors":"Lan Wu, Zhi-Zheng Li, Hao Yang, Li-Zhi Cao, Xiao-Ying Wang, Dong-Liang Wang, Emeli Chatterjee, Yan-Fei Li, Gang Huang","doi":"10.1007/s00395-024-01076-8","DOIUrl":"10.1007/s00395-024-01076-8","url":null,"abstract":"Exercise is an effective way to alleviate breast cancer-induced cardiac injury to a certain extent. However, whether voluntary exercise (VE) activates cardiac signal transducer and activator of transcription 3 (STAT3) and the underlying mechanisms remain unclear. This study investigated the role of STAT3-microRNA(miRNA)-targeted protein axis in VE against breast cancer-induced cardiac injury.VE for 4 weeks not only improved cardiac function of transgenic breast cancer female mice [mouse mammary tumor virus-polyomavirus middle T antigen (MMTV-PyMT +)] compared with littermate mice with no cancer (MMTV-PyMT -), but also increased myocardial STAT3 tyrosine 705 phosphorylation. Significantly more obvious cardiac fibrosis, smaller cardiomyocyte size, lower cell viability, and higher serum tumor necrosis factor (TNF)-α were shown in MMTV-PyMT + mice compared with MMTV-PyMT - mice, which were ameliorated by VE. However, VE did not influence the tumor growth. MiRNA sequencing identified that miR-181a-5p was upregulated and miR-130b-3p was downregulated in VE induced-cardioprotection. Myocardial injection of Adeno-associated virus serotype 9 driving STAT3 tyrosine 705 mutations abolished cardioprotective effects above. Myocardial STAT3 was identified as the transcription factor binding the promoters of pri-miR-181a (the precursor of miR-181a-5p) and HOX transcript antisense RNA (HOTAIR, sponged miR-130b-3p) in isolated cardiomyocytes. Furthermore, miR-181a-5p targeting PTEN and miR-130b-3p targeting Zinc finger and BTB domain containing protein 20 (Zbtb20) were proved in AC-16 cells. These findings indicated that VE protects against breast cancer-induced cardiac injury via activating STAT3 to promote miR-181a-5p targeting PTEN and to promote HOTAIR to sponge miR-130b-3p targeting Zbtb20, helping to develop new targets in exercise therapy for breast cancer-induced cardiac injury.","PeriodicalId":8723,"journal":{"name":"Basic Research in Cardiology","volume":" ","pages":"113-131"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141999391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Preclinical models of cardiotoxicity from immune checkpoint inhibitor therapy. 免疫检查点抑制剂疗法心脏毒性的临床前模型。

IF 7.5 1区医学

Basic Research in Cardiology Pub Date : 2025-02-01 Epub Date: 2024-07-22 DOI: 10.1007/s00395-024-01070-0

Florian Buehning, Tobias Lerchner, Julia Vogel, Ulrike B Hendgen-Cotta, Matthias Totzeck, Tienush Rassaf, Lars Michel

{"title":"Preclinical models of cardiotoxicity from immune checkpoint inhibitor therapy.","authors":"Florian Buehning, Tobias Lerchner, Julia Vogel, Ulrike B Hendgen-Cotta, Matthias Totzeck, Tienush Rassaf, Lars Michel","doi":"10.1007/s00395-024-01070-0","DOIUrl":"10.1007/s00395-024-01070-0","url":null,"abstract":"Immune checkpoint inhibitor (ICI) therapy represents a ground-breaking paradigm in cancer treatment, harnessing the immune system to combat malignancies by targeting checkpoints such as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1). The use of ICI therapy generates distinctive immune-related adverse events (irAEs) including cardiovascular toxicity, necessitating targeted research efforts. This comprehensive review explores preclinical models dedicated to ICI-mediated cardiovascular complications including myocarditis. Tailored preclinical models of ICI-mediated myocardial toxicities highlight the key role of CD8+ T cells, emphasizing the profound impact of immune checkpoints on maintaining cardiac integrity. Cytokines and macrophages were identified as possible driving factors in disease progression, and at the same time, initial data on possible cardiac antigens responsible are emerging. The implications of contributing factors including thoracic radiation, autoimmune disorder, and the presence of cancer itself are increasingly understood. Besides myocarditis, mouse models unveiled an accelerated progression of atherosclerosis, adding another layer for a thorough understanding of the diverse processes involving cardiovascular immune checkpoint signalling. This review aims to discuss current preclinical models of ICI cardiotoxicity and their potential for improving enhanced risk assessment and diagnostics, offering potential targets for innovative cardioprotective strategies. Lessons from ICI therapy can drive novel approaches in cardiovascular research, extending insights to areas such as myocardial infarction and heart failure.","PeriodicalId":8723,"journal":{"name":"Basic Research in Cardiology","volume":" ","pages":"171-185"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141750195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sodium-glucose cotransporter 2 inhibitors and the cancer patient: from diabetes to cardioprotection and beyond. 钠-葡萄糖共转运体 2 抑制剂与癌症患者：从糖尿病到心脏保护及其他。

IF 7.5 1区医学

Basic Research in Cardiology Pub Date : 2025-02-01 Epub Date: 2024-06-27 DOI: 10.1007/s00395-024-01059-9

Massimiliano Camilli, Marcello Viscovo, Luca Maggio, Alice Bonanni, Ilaria Torre, Claudio Pellegrino, Priscilla Lamendola, Lorenzo Tinti, Luciana Teofili, Stefan Hohaus, Gaetano Antonio Lanza, Peter Ferdinandy, Zoltan Varga, Filippo Crea, Antonella Lombardo, Giorgio Minotti

{"title":"Sodium-glucose cotransporter 2 inhibitors and the cancer patient: from diabetes to cardioprotection and beyond.","authors":"Massimiliano Camilli, Marcello Viscovo, Luca Maggio, Alice Bonanni, Ilaria Torre, Claudio Pellegrino, Priscilla Lamendola, Lorenzo Tinti, Luciana Teofili, Stefan Hohaus, Gaetano Antonio Lanza, Peter Ferdinandy, Zoltan Varga, Filippo Crea, Antonella Lombardo, Giorgio Minotti","doi":"10.1007/s00395-024-01059-9","DOIUrl":"10.1007/s00395-024-01059-9","url":null,"abstract":"Sodium-glucose cotransporter 2 inhibitors (SGLT2i), a new drug class initially designed and approved for treatment of diabetes mellitus, have been shown to exert pleiotropic metabolic and direct cardioprotective and nephroprotective effects that extend beyond their glucose-lowering action. These properties prompted their use in two frequently intertwined conditions, heart failure and chronic kidney disease. Their unique mechanism of action makes SGLT2i an attractive option also to lower the rate of cardiac events and improve overall survival of oncological patients with preexisting cardiovascular risk and/or candidate to receive cardiotoxic therapies. This review will cover biological foundations and clinical evidence for SGLT2i modulating myocardial function and metabolism, with a focus on their possible use as cardioprotective agents in the cardio-oncology settings. Furthermore, we will explore recently emerged SGLT2i effects on hematopoiesis and immune system, carrying the potential of attenuating tumor growth and chemotherapy-induced cytopenias.","PeriodicalId":8723,"journal":{"name":"Basic Research in Cardiology","volume":" ","pages":"241-262"},"PeriodicalIF":7.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11790819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141454981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bridging cardiology and oncology in the era of precision medicine.

IF 7.5 1区医学

Basic Research in Cardiology Pub Date : 2025-02-01 Epub Date: 2025-02-03 DOI: 10.1007/s00395-025-01097-x

Tienush Rassaf

引用次数: 0