2026-04-30T10:43:38Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/111202024-09-27T08:29:14Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
González-Ramos, Silvia
author
Fernández-García, Victoria
author
Recalde, Miriam
author
Rodriguez, Cristina
author
Martinez-Gonzalez, Jose
author
Andres, Vicente
author
Martín-Sanz, Paloma
author
Boscá, Lisardo
funder
Ministerio de Ciencia, Innovación y Universidades (España)
funder
Centro de Investigación Biomedica en Red - CIBER
funder
Fundación Ramón Areces
funder
Comunidad de Madrid (España)
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
funder
Fundación ProCNIC
2020-10-08T10:26:08Z
2020-10-08T10:26:08Z
2020-09-10
Cells. 2020; 9(9):e2067
10.3390/cells9092067
2073-4409
Cells
32927803
http://hdl.handle.net/20.500.12105/11120
Atherothrombosis, the main cause of acute coronary syndromes (ACS), is characterized by the rupture of the atherosclerotic plaque followed by the formation of thrombi. Fatal plaque rupture sites show large necrotic cores combined with high levels of inflammation and thin layers of collagen. Plaque necrosis due to the death of macrophages and smooth muscle cells (SMCs) remains critical in the process. To determine the contribution of the innate immunity receptor NOD1 to the stability of atherosclerotic plaque, Apoe-/- and Apoe-/- Nod1-/- atherosclerosis prone mice were placed on a high-fat diet for 16 weeks to assess post-mortem advanced atherosclerosis in the aortic sinus. The proliferation and apoptosis activity were analyzed, as well as the foam cell formation capacity in these lesions and in primary cultures of macrophages and vascular SMCs obtained from both groups of mice. Our results reinforce the preeminent role for NOD1 in human atherosclerosis. Advanced plaque analysis in the Apoe-/- atherosclerosis model suggests that NOD1 deficiency may decrease the risk of atherothrombosis by decreasing leukocyte infiltration and reducing macrophage apoptosis. Furthermore, Nod1-/- SMCs exhibit higher proliferation rates and decreased apoptotic activity, contributing to thicker fibrous caps with reduced content of pro-thrombotic collagen. These findings demonstrate a direct link between NOD1 and plaque vulnerability through effects on both macrophages and SMCs, suggesting promising insights for early detection of biomarkers for treating patients before ACS occurs.
eng
Deletion or Inhibition of NOD1 Favors Plaque Stability and Attenuates Atherothrombosis in Advanced Atherogenesis †.
journal article
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DeletionOrInhibitionNOD1Favors_2020.pdf
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DeletionOrInhibitionNOD1Favors_2020_s001.pdf
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DeletionOrInhibitionNOD1Favors_2020.pdf.txt
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DeletionOrInhibitionNOD1Favors_2020_s001.pdf.txt