PhD Scientific Days 2024

Budapest, 9-10 July 2024

Poster Session N - Cardiovascular Medicine and Research 2.

Inflammaging: Impact of Inflammation on Cardiopulmonary Decline in Old Mice

Text of the abstract

Introduction: Population aging is a global phenomenon with a noticeable growth every year. The prevalence of age-related cardiovascular diseases is highly associated with advancing age. Chronic low-grade inflammation, termed inflammaging, emerged as a risk factor for multiple diseases in elderly individuals. At such pro-inflammatory status, the level of multiprotein complexes (inflammasomes) is altered, and that correlates with health and disease during aging.

Aims: Given the increase in life expectancy, further understanding of the inflammatory background in aging is crucial. We aim to assess if inhibiting a wide array of inflammasomes can ameliorate cardiovascular dysfunction in the older population.

Methods: We treated 90-week-old C57Bl/6J mice with Canakinumab, Probenecid or vehicle for six months. At the beginning of the study and before the termination, we performed echocardiography. After the treatment period, we terminated all the mice and collected their organs (heart, lung, kidney, liver, spleen, pancreas, adrenal gland and brain). One part of the collected sample was placed in Formalin for histological examination. The other part was frozen in liquid Nitrogen and then stored at -80 C for further experiments (ELISA, Western Blot).

Result: Our results did not show a significant difference in the Echocardiography parameters between groups, apart from mild improvement in the ejection fraction in the canakinumab-treated mice. Histological analysis of liver samples showed no significant difference in the percentage of the fibrotic area between the treated and control groups.

Conclusion: our current study investigated the potential role of selective and non-selective inflammasome inhibition in improving the cardiovascular system in the aged population. While our results did not show a significant effect, we aim to further investigate the role of inflammasomes (e.g., NLRC4, AIM2, NLRP1 and NLRP3 ) and downstream mediators in developing low-grade inflammation in the aged heart.