Roa-Bruzón Iliannis Y, Duany-Almira Luis F, Valle-Delgadillo Yeminia M, Flores-Salinas Héctor E, Valdés-Alvarado Emmanuel, Padilla-Gutiérrez Jorge R
Centro Universitario de Ciencias de la Salud, Instituto de Investigación en Ciencias Biomédicas (IICB), Universidad de Guadalajara, Guadalajara 44340, Jalisco, Mexico.
Departamento de Biología Molecular y Genómica, Universidad de Guadalajara, Guadalajara 44340, Jalisco, Mexico.
Cells. 2025 Apr 15;14(8):597. doi: 10.3390/cells14080597.
Ankylosing spondylitis (AS) is a chronic inflammatory disease that primarily affects the joints, limiting patients' mobility and quality of life. Recent studies have shown that patients with AS have a significantly higher risk of developing severe cardiovascular complications, such as acute coronary syndrome (ACS). A comprehensive review (2014-2024) included a study evaluating the significance of matrix metalloproteinase 3 (MMP-3) in cardiovascular risk among AS patients. The findings indicate that chronic inflammation in AS not only damages the joints but also contributes to the progression of cardiovascular diseases. At the molecular level, MMP-3 is instrumental in degrading the extracellular matrix, leading to instability in the atherosclerotic plaques and increasing the risk of ACS. Additionally, MMP-3 activation is related to the inflammatory pathways, such as tumor necrosis factor-alpha (TNF-α) and NF-κB, which amplify its effect on both joint destruction and vascular damage. This molecular approach offers new perspectives for understanding and treating AS and its cardiovascular complications, suggesting that MMP-3 inhibition could be a promising therapeutic strategy to mitigate cardiovascular risk in these patients.
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