Fuster JJ*, Zuriaga MA, Zorita V, MacLauchlan S, Polackal MN, Viana-Huete V, Ferrer-Perez A, Matesanz N, Herrero-Cervera A, Sano S, Cooper MA, Gonzalez-Navarro H, Walsh K* (*co-correspondig authors)
Menu
Most deaths in the world are caused by damage to the cardiovascular system, with atherosclerosis (inflammation of large vessels) representing the main underlying cause of cardiovascular disease (CVD).
Clonal Hematopoiseis (CH) represents a clonal expansion of blood cells arising from somatic mutations in genes that confer a growth advantage to hematopoietic stem cells (HSCs) and were therefore associated with the onset of blood cancers.
Members form our Network demonstrated that CH increases in frequency from age 40 onwards, is present in >10% of people aged >70 and increases risk of myocardial infarction by at least 2-3 fold, suggesting that CH could be the most important non-traditional risk factor underlying atherosclerotic CVD.
CH usually involves mutations in one of four genes producing loss of function in epigenetic modifiers (TET2, ASXL1 or DNMT3A) or increased hematopoietic signaling (JAK2) that typically alter the function rather than the number of inflammatory cells, including macrophages, monocytes, neutrophils and platelets.
We propose that CH mutations has adverse effects on the functions of these cells that could lead to athero-thrombosis. Our Network will use multiple approaches to better understand how the atherosclerotic plaque forms, its relation with CH, and examine strategies to alleviate vascular inflammation and CVD.
Use this form to contact us. We respond as soon as possible.
In accordance with the provisions of the General Data Protection Regulation (GDPR) (EU) 2016/679, we hereby inform you that personal information you provide via this contact form will be registered and incorporated in the database-management systems managed by the Centro Nacional de Investigaciones Cardiovasculares Carlos III (F.S.P.) in order to ensure the prompt and effective processing of your request. If you decline consent for the incorporation of your personal data in our database-management systems, we will be unable to process your request.
We further inform you that we will not use personal information you provide for any other purpose than the completion of your request, and nor will we communicate your personal information to any third party unless we are required to do so by law or unless we have you express authorization to do so.
You can exercise your rights to access, rectify, delete, or transfer your personal information or limit or oppose any specific aspect of its handling by writing to the Centro Nacional de Investigaciones Cardiovasculares C/ Melchor Fernández Almagro 3, Madrid 28029, Spain. To obtain more information about how we handle your personal data and to access our forms developed to assist you in exercising your rights, please consult the privacy section of our website: https://www.cnic.es/en/privacy
