Blocking Interleukin-1 Beta Reduces the Evolution of Thoracic Aortic Dissection in a Rodent Model

Area of Science:

• Cardiovascular Biology
• Pathology
• Molecular Medicine

Background:

• Thoracic aortic dissection (TAD) involves matrix and biochemical changes, with interleukin-1 beta (IL-1β) implicated.
• The precise mechanisms driving TAD development, including the roles of IL-1β, matrix metalloproteinases (MMPs), apoptosis, and elastic fiber integrity, remain unclear.

Purpose of the Study:

• To investigate the role of IL-1β in TAD development using a rat model.
• To examine the impact of IL-1β and its antibody on MMP-2, MMP-9, smooth muscle cell apoptosis, elastic fiber fracture, and biomechanical properties in TAD.

Main Methods:

• A thoracic aortic dissection (TAD) rat model was established using β-aminopropionitrile (BAPN).
• Rats were divided into control, BAPN, BAPN + IL-1β, and BAPN + IL-1β antibody groups.
• Measurements included mortality, TAD development, IL-1β, MMP-2, MMP-9 expression, apoptosis, elastin content, and biomechanical characteristics.

Main Results:

• IL-1β administration significantly increased mortality and aneurysm expansion in the BAPN-induced TAD model.
• IL-1β treatment led to decreased stress/strain parameters and elastin content, alongside elevated IL-1β, MMP-2, and MMP-9 expression.
• Anti-IL-1β treatment attenuated these detrimental effects, partially or completely reversing the observed changes.

Conclusions:

• Interleukin-1 beta (IL-1β) critically contributes to thoracic aortic dissection (TAD) pathogenesis.
• IL-1β promotes TAD by increasing MMP expression, degrading the aortic wall, and altering biomechanical properties.
• Targeting IL-1β with antibodies presents a potential therapeutic strategy for TAD prognosis and treatment.