A disturbance of the structure of the aortic wall results in the formation of aortic aneurysm, which is characterized by a significant bulge on the vessel surface that may have consequences, such as distention and finally rupture. Abdominal aortic aneurysm (AAA) is a major pathological condition because it affects approximately 8% of elderly men and 1.5% of elderly women. The pathogenesis of AAA involves multiple interlocking mechanisms, including inflammation, immune cell activation, protein degradation and cellular malalignments. The expression of inflammatory factors, such as cytokines and chemokines, induce the infiltration of inflammatory cells into the wall of the aorta, including macrophages, natural killer cells (NK cells) and T and B lymphocytes. Protein degradation occurs with a high expression not only of matrix metalloproteinases (MMPs) but also of neutrophil gelatinase-associated lipocalin (NGAL), interferon gamma (IFN-γ) and chymases. The loss of extracellular matrix (ECM) due to cell apoptosis and phenotype switching reduces tissue density and may contribute to AAA. It is important to consider the key mechanisms of initiating and promoting AAA to achieve better preventative and therapeutic outcomes.

Department of Obstetrics and Gynecology University Hospital and Masaryk University 602 00 Brno Czech Republic

Department of Physiotherapy University School of Physical Education 51 612 Wroclaw Poland

Division of Anatomy and Histology University of Zielona Góra 65 046 Zielona Góra Poland

Division of Anatomy Department of Human Morphology and Embryology Wroclaw Medical University 50 368 Wroclaw Poland

Division of Histology and Embryology Department of Human Morphology and Embryology Wroclaw Medical University 50 368 Wroclaw Poland

Fertility Infertility and Perinatology Research Center Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran

Institute of Veterinary Medicine Nicolaus Copernicus University 87 100 Torun Poland

Physiology Graduate Faculty North Carolina State University Raleigh NC 27613 USA

Prestage Department of Poultry Science North Carolina State University Raleigh NC 27607 USA

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$a A disturbance of the structure of the aortic wall results in the formation of aortic aneurysm, which is characterized by a significant bulge on the vessel surface that may have consequences, such as distention and finally rupture. Abdominal aortic aneurysm (AAA) is a major pathological condition because it affects approximately 8% of elderly men and 1.5% of elderly women. The pathogenesis of AAA involves multiple interlocking mechanisms, including inflammation, immune cell activation, protein degradation and cellular malalignments. The expression of inflammatory factors, such as cytokines and chemokines, induce the infiltration of inflammatory cells into the wall of the aorta, including macrophages, natural killer cells (NK cells) and T and B lymphocytes. Protein degradation occurs with a high expression not only of matrix metalloproteinases (MMPs) but also of neutrophil gelatinase-associated lipocalin (NGAL), interferon gamma (IFN-γ) and chymases. The loss of extracellular matrix (ECM) due to cell apoptosis and phenotype switching reduces tissue density and may contribute to AAA. It is important to consider the key mechanisms of initiating and promoting AAA to achieve better preventative and therapeutic outcomes.

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