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Identified a new mechanism involved in the development of atherosclerotic injury

The Cardiovascular Risk Metabolic Basis Research Group of the Sant Pau-IIB Sant Pau Research Institute, attached to CIBERDEM, is collaborating on research which identifies a new mechanism involved in the development of atherosclerotic lesions.

Reference article

Cardiovascular disease, and in particular atherosclerosis, is one of the leading causes of death in adults in Western countries. Therefore, studying this pathology is fundamental and in this line, researchers from the CIBER of Cardiovascular Diseases (CIBERCV) of Luis Miguel Blanco Colio’s group at the Fundación Jiménez Díaz Health Research Institute have identified a new mechanism involved in the development of these lesions. In a study published in the FASEB Journal, in which they have collaborated with the group of Jesús Egido (Fundación Jiménez Díaz) and Joan Carles Escolà-Gil (Sant Pau Research Institute-IIB Sant Pau) of the CIBER of the Cardiovascular Risk Metabolic Basis (CIBERDEM), the researchers have analysed the role played by the CD163 protein, specific to one type of inflammatory cell, macrophages, in the progression of atherosclerotic lesions. This disease consists of the progressive accumulation of cholesterol and inflammatory cells in the arterial wall giving rise to atherosclerotic plaque which, in advanced stages, can lead to death due to myocardial infarction or cerebral ictus.


A new study on genetically modified mica

Researchers have studied the mechanisms through which the macrophage receptor CD163 – cells of the immune system that intervene in the body’s defence to eliminate foreign substances, excess or pathogenic agents – regulates the development of atherosclerotic lesions. In this work, thanks to genetically modified mice, they have detected that the presence of these anti-inflammatory macrophages that express this protein are essential to prevent the progression of this disease. According to the first signatory of the article, Carmen Gutiérrez, they have demonstrated that the absence of CD163 favours the accumulation of lipids in cells and therefore favours the evolution of the disease. “Deficiency in this protein is associated with an increase in a receptor (CD36) for bad cholesterol (LDL), leading to an increase in the accumulation of lipids inside the atherosclerotic lesion, making the plaques progress more rapidly and more prone to rupture”. Therefore, indicates CIBERCV researcher Nerea Méndez and co-author of the work, “the increase of CD163 expression in macrophages could be a new therapeutic target for the treatment of atherosclerosis, due to its protective role during the progression of this disease”.


Reference article:

CD163 deficiency increases foam cell formation and plaque progression in atherosclerotic mice Carmen Gutiérrez-Muñoz, Nerea Méndez-Barbero, Pia Svendsen, Cristina Sastre,  Valvanera Fernández-Laso, Patricia Quesada, Jesús Egido, Joan C. Escolá-Gil, Jose L. Martín-Ventura, Soren K. Moestrup, Luis M. Blanco-Colio FASEB J 2020. doi: 10.1096/fj.202000177R.

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